{"gene":"SAPCD2","run_date":"2026-06-10T07:46:29","timeline":{"discoveries":[{"year":2016,"finding":"SAPCD2 (p42.3) physically interacts with LGN and negatively regulates LGN localization at the cell cortex, likely by competing with NuMA for LGN binding, thereby controlling mitotic spindle orientation in epithelial cells and mouse retinal progenitor cells in vivo.","method":"Co-IP/pulldown to identify LGN as binding partner; siRNA loss-of-function in epithelial cyst cultures and in vivo retinal progenitor assays; competition binding assays with NuMA","journal":"Developmental cell","confidence":"High","confidence_rationale":"Tier 2 / Strong — reciprocal binding assays, clean KO/KD with defined cellular and in vivo phenotypes (spindle misorientation, cyst morphogenesis defects, tripled asymmetric divisions), multiple orthogonal methods across cell culture and animal model","pmids":["26766442"],"is_preprint":false},{"year":2026,"finding":"SAPCD2 functions as a microtubule-associated protein that promotes microtubule stability; CDK1-mediated phosphorylation at S157, together with phosphorylation at S276, generates a mitosis-specific isoform that destabilizes astral microtubules to control spindle orientation. Disruption of phosphorylation at both S157 and S276 fails to rescue spindle misorientation caused by SAPCD2 depletion.","method":"Live-cell imaging; siRNA depletion; phospho-site mutagenesis (S157A, S276A); microtubule stability assays; identification of CDK1 as the kinase for S157","journal":"Communications biology","confidence":"High","confidence_rationale":"Tier 1–2 / Moderate — phospho-site mutagenesis combined with live-cell imaging, in vitro kinase identification (CDK1), and functional rescue experiments in a single rigorous study","pmids":["42151476"],"is_preprint":false},{"year":2018,"finding":"C9orf140 (SAPCD2) is a negative regulator of Wnt/β-catenin signaling that interacts with Axin1, outcompetes PP2A for Axin1 binding, thereby shifting the balance toward phosphorylation of β-catenin and reducing Wnt3A-induced β-catenin accumulation. Wnt signaling in turn induces C9orf140 expression via β-catenin, forming a negative feedback loop.","method":"Tandem-affinity purification and mass spectrometry to identify Axin1 as binding partner; Co-IP; competition assay with PP2A; β-catenin phosphorylation assays in cultured cells; zebrafish embryo functional validation","journal":"Oncogene","confidence":"High","confidence_rationale":"Tier 1–2 / Strong — TAP-MS identification of binding partner, Co-IP, competition binding, functional phosphorylation assays, and in vivo zebrafish epistasis in a single study with multiple orthogonal methods","pmids":["29531269"],"is_preprint":false},{"year":2007,"finding":"p42.3 (SAPCD2) expression is cell cycle-dependent in gastric cancer cell lines, with peak expression at M phase. RNAi-mediated depletion causes G2/M arrest, suppresses cell proliferation and tumorigenicity, and alters expression of cyclin B1 and Chk2.","method":"Cell cycle synchronization + RT-PCR/Western blot; siRNA knockdown; colony formation and xenograft tumorigenicity assays; flow cytometry","journal":"Oncogene","confidence":"Medium","confidence_rationale":"Tier 2 / Moderate — clean KD with defined cell cycle phenotype and downstream marker changes, single lab, two orthogonal functional assays","pmids":["17525738"],"is_preprint":false},{"year":2012,"finding":"p42.3 (SAPCD2) overexpression in NIH3T3 cells promotes malignant transformation with accelerated mitotic progression, altered chromosome segregation, upregulation of Cyclin B1, and downregulation of Cdc2-Tyr15 phosphorylation.","method":"Stable transfection of p42.3 into NIH3T3 cells; Western blot for cell cycle proteins; mitotic progression assays","journal":"Molecular carcinogenesis","confidence":"Medium","confidence_rationale":"Tier 2 / Moderate — gain-of-function with defined molecular readouts (Cyclin B1, Cdc2-Tyr15), single lab, multiple assay types","pmids":["23192843"],"is_preprint":false},{"year":2022,"finding":"SAPCD2 directly binds cytoplasmic E2F7 (but not E2F1) and alters its subcellular distribution; SAPCD2 knockdown increases nuclear E2F7 accumulation, thereby affecting expression of genes involved in cell cycle regulation and chromosome instability in neuroblastoma cells.","method":"Co-IP to demonstrate direct SAPCD2–E2F7 (not E2F1) binding; subcellular fractionation; siRNA knockdown with gene expression profiling; in vitro and in vivo functional assays","journal":"Cell death & disease","confidence":"Medium","confidence_rationale":"Tier 2 / Moderate — Co-IP binding assay, subcellular fractionation showing redistribution of E2F7, KD phenotype with pathway-level readout, single lab","pmids":["35197448"],"is_preprint":false},{"year":2011,"finding":"miR-29a directly binds the 3′UTR of p42.3 (SAPCD2) mRNA to repress p42.3 expression at both mRNA and protein levels, inducing cell cycle arrest and inhibiting proliferation in gastric cancer cells.","method":"3′UTR luciferase reporter assay; Western blot and qRT-PCR; miR-29a mimic transfection; cell cycle analysis","journal":"PloS one","confidence":"Medium","confidence_rationale":"Tier 2 / Moderate — direct 3′UTR reporter validation of miRNA-mRNA interaction, functional cell cycle readout, single lab","pmids":["21998710"],"is_preprint":false},{"year":2020,"finding":"Silencing SAPCD2 in fibrosarcoma cells activates the Hippo signaling pathway (reduces YAP1 activity); constitutively active YAP1-S127A rescues the inhibitory effects of SAPCD2 knockdown on colony formation, anchorage-independent growth, and apoptosis, placing SAPCD2 upstream of YAP1 in this pathway.","method":"siRNA knockdown; genetic epistasis with YAP1-S127A rescue construct; colony formation and anchorage-independent growth assays; apoptosis assay; in vivo lung metastasis model","journal":"Frontiers in oncology","confidence":"Medium","confidence_rationale":"Tier 2 / Moderate — genetic epistasis (YAP1-S127A rescue) establishes pathway position, complemented by in vivo model, single lab","pmids":["33384953"],"is_preprint":false},{"year":2020,"finding":"SAPCD2 knockdown in breast cancer cells reduces YAP/TAZ protein expression and inhibits proliferation, migration, and invasion; simultaneous YAP overexpression reverses these effects, placing SAPCD2 upstream of YAP/TAZ.","method":"siRNA knockdown; YAP overexpression rescue; Western blot for YAP/TAZ; CCK-8, transwell assays","journal":"European review for medical and pharmacological sciences","confidence":"Low","confidence_rationale":"Tier 3 / Weak — single lab, rescue experiment shows epistatic relationship but mechanistic link between SAPCD2 and YAP/TAZ is not biochemically characterized","pmids":["32329855"],"is_preprint":false},{"year":2019,"finding":"LncRNA PXN-AS1-L directly interacts with SAPCD2 mRNA 3′UTR to prevent miRNA-AGO silencing complex binding, thereby upregulating SAPCD2 mRNA and protein levels in nasopharyngeal carcinoma cells.","method":"RNA pull-down / RNA-RNA interaction assay; qRT-PCR and Western blot; SAPCD2 depletion rescue experiments in vitro and in vivo","journal":"Cancer medicine","confidence":"Low","confidence_rationale":"Tier 3 / Weak — RNA-RNA interaction proposed and supported by pulldown, but AGO competition mechanism not biochemically reconstituted; single lab","pmids":["31173488"],"is_preprint":false},{"year":2026,"finding":"SAPCD2 stabilizes TANK protein by preventing its ubiquitin-mediated degradation by SYVN1, activates MAPK signaling, and through CREB phosphorylation enhances PLAGL2 expression, which in turn amplifies SAPCD2 expression in a positive feedback loop driving bladder cancer progression.","method":"Co-IP; ubiquitination assays; CREB phosphorylation assays; siRNA/overexpression functional assays; in vivo tumor models","journal":"Cancers","confidence":"Low","confidence_rationale":"Tier 3 / Weak — mechanistic claims from a single lab with Co-IP and phosphorylation assays, but abstract provides limited methodological detail on reconstitution or mutagenesis","pmids":["41682005"],"is_preprint":false},{"year":2014,"finding":"STAT5 directly interacts with EZH2 and β-catenin to enhance C9orf140 (SAPCD2) gene transactivation, and C9orf140 promotes epithelial-mesenchymal transition and CRC cell invasion downstream of STAT5, EZH2, and β-catenin.","method":"siRNA knockdown and overexpression; Co-IP for STAT5-EZH2-β-catenin interaction; EMT marker analysis; in vivo metastasis model","journal":"Carcinogenesis","confidence":"Low","confidence_rationale":"Tier 3 / Weak — Co-IP for upstream complex, KD/OE with pathway readout, single lab, mechanistic details limited in abstract","pmids":["24608043"],"is_preprint":false},{"year":2023,"finding":"SAPCD2 protein is localized predominantly in the cytoplasm of CRC cells, as determined by immunofluorescence with SAPCD2-EGFP recombinant constructs.","method":"Immunofluorescence with SAPCD2-EGFP fusion constructs in HCT116 cells","journal":"Cellular and molecular biology","confidence":"Low","confidence_rationale":"Tier 3 / Weak — direct localization by fluorescent construct, single lab, no functional consequence linked to localization","pmids":["38158695"],"is_preprint":false}],"current_model":"SAPCD2 (p42.3/C9orf140) is a cell cycle-regulated protein that functions as a microtubule-associated protein controlling astral microtubule stability and mitotic spindle orientation: its activity is toggled by CDK1-mediated phosphorylation at S157 (and S276), creating a mitosis-specific isoform that destabilizes astral microtubules; it also directly binds LGN and competes with NuMA to limit cortical LGN accumulation, thereby restraining planar spindle orientation during epithelial morphogenesis and asymmetric cell division; additionally, SAPCD2 interacts with Axin1 to outcompete PP2A, shifting β-catenin toward phosphorylation and acting as a negative feedback regulator of Wnt/β-catenin signaling; in cancer contexts it binds cytoplasmic E2F7 to restrict its nuclear accumulation, activates YAP/TAZ and Hippo pathway components, and stabilizes TANK to sustain MAPK signaling, while its own expression is post-transcriptionally regulated by miR-29a and miR-486-5p via 3′UTR binding."},"narrative":{"mechanistic_narrative":"SAPCD2 (p42.3/C9orf140) is a cell cycle-regulated, cytoplasmic protein that controls mitotic spindle orientation by acting as a microtubule-associated protein [PMID:42151476, PMID:17525738]. It directly binds LGN and negatively regulates LGN accumulation at the cell cortex, competing with NuMA to limit cortical LGN and thereby restraining planar spindle orientation during epithelial morphogenesis and asymmetric division of retinal progenitors [PMID:26766442]. CDK1-mediated phosphorylation at S157, together with phosphorylation at S276, generates a mitosis-specific isoform that destabilizes astral microtubules; disruption of both sites prevents rescue of the spindle misorientation caused by SAPCD2 loss [PMID:42151476]. Independently, SAPCD2 acts as a negative-feedback regulator of Wnt/β-catenin signaling by binding Axin1 and outcompeting PP2A, shifting β-catenin toward phosphorylation, while Wnt signaling itself induces SAPCD2 expression [PMID:29531269]. In cancer contexts SAPCD2 drives proliferation and tumorigenicity, with expression peaking at M phase and depletion causing G2/M arrest [PMID:17525738]; it directly binds cytoplasmic E2F7 to restrict its nuclear accumulation [PMID:35197448] and operates upstream of YAP1 to regulate Hippo-pathway-dependent growth [PMID:33384953]. Its expression is post-transcriptionally repressed by miR-29a binding the 3′UTR [PMID:21998710].","teleology":[{"year":2007,"claim":"Established SAPCD2 (p42.3) as a cell cycle-dependent, proliferation-promoting protein, defining its first functional context before any molecular mechanism was known.","evidence":"Cell cycle synchronization with RT-PCR/Western, siRNA knockdown, colony formation and xenograft assays in gastric cancer cells","pmids":["17525738"],"confidence":"Medium","gaps":["No molecular partner or biochemical activity identified","Mechanism linking SAPCD2 to cyclin B1/Chk2 changes unresolved"]},{"year":2011,"claim":"Identified an upstream regulatory input by showing miR-29a directly represses SAPCD2 via its 3′UTR, placing SAPCD2 within a defined post-transcriptional control axis.","evidence":"3′UTR luciferase reporter, miR-29a mimic, Western/qRT-PCR and cell cycle analysis in gastric cancer cells","pmids":["21998710"],"confidence":"Medium","gaps":["Does not address downstream effector function of SAPCD2","Only one regulatory miRNA tested"]},{"year":2012,"claim":"Demonstrated SAPCD2 is oncogenic gain-of-function, accelerating mitotic progression and altering chromosome segregation, reinforcing a mitotic role.","evidence":"Stable overexpression in NIH3T3 cells with cell cycle protein Western blots and mitotic progression assays","pmids":["23192843"],"confidence":"Medium","gaps":["No direct molecular target of SAPCD2 identified","Mechanism of altered segregation not defined"]},{"year":2016,"claim":"Provided the first direct molecular mechanism: SAPCD2 binds LGN and competes with NuMA to limit cortical LGN, controlling spindle orientation and asymmetric division in vivo.","evidence":"Co-IP/pulldown, NuMA competition assays, siRNA in epithelial cysts and mouse retinal progenitors","pmids":["26766442"],"confidence":"High","gaps":["Structural basis of LGN binding not resolved","Did not establish how SAPCD2 itself is recruited to the cortex"]},{"year":2018,"claim":"Revealed a distinct signaling function as a negative-feedback regulator of Wnt/β-catenin through Axin1 binding and PP2A competition.","evidence":"TAP-MS, Co-IP, PP2A competition, β-catenin phosphorylation assays, zebrafish epistasis","pmids":["29531269"],"confidence":"High","gaps":["Relationship between Wnt-regulatory and spindle-orientation functions unclear","No structural detail of the Axin1 interaction"]},{"year":2022,"claim":"Showed SAPCD2 directly binds cytoplasmic E2F7 and restricts its nuclear accumulation, linking SAPCD2 to transcriptional control of cell cycle and chromosome stability genes.","evidence":"Co-IP (E2F7-specific, not E2F1), subcellular fractionation, siRNA with expression profiling in neuroblastoma","pmids":["35197448"],"confidence":"Medium","gaps":["Mechanism of cytoplasmic sequestration not defined","Reciprocal validation of binding limited"]},{"year":2026,"claim":"Defined the mitotic switch mechanism: CDK1 phosphorylates SAPCD2 at S157 (with S276) to create a microtubule-destabilizing, mitosis-specific isoform required for correct spindle orientation.","evidence":"Live-cell imaging, phospho-site mutagenesis (S157A, S276A), in vitro CDK1 kinase identification, rescue experiments","pmids":["42151476"],"confidence":"High","gaps":["Structural basis of microtubule binding unresolved","How phosphorylation alters microtubule association mechanistically not shown"]},{"year":null,"claim":"It remains unclear how SAPCD2's distinct activities — astral microtubule destabilization, cortical LGN competition, Wnt/Axin1 feedback, and E2F7/YAP regulation — are integrated within a single cell or coordinated across cell-cycle stages.","evidence":"No single study reconciles the spindle-orientation and signaling roles","pmids":[],"confidence":"Low","gaps":["No structural model of SAPCD2","No unified framework connecting its microtubule and signaling functions","Domain architecture mediating the multiple interactions undefined"]}],"mechanism_profile":{"molecular_activity":[{"term_id":"GO:0008092","term_label":"cytoskeletal protein binding","supporting_discovery_ids":[1]},{"term_id":"GO:0098772","term_label":"molecular function regulator activity","supporting_discovery_ids":[0,2]}],"localization":[{"term_id":"GO:0005829","term_label":"cytosol","supporting_discovery_ids":[12,5]},{"term_id":"GO:0005856","term_label":"cytoskeleton","supporting_discovery_ids":[1]}],"pathway":[{"term_id":"R-HSA-1640170","term_label":"Cell Cycle","supporting_discovery_ids":[1,3]},{"term_id":"R-HSA-162582","term_label":"Signal Transduction","supporting_discovery_ids":[2]}],"complexes":[],"partners":["LGN","NUMA","AXIN1","PP2A","E2F7"],"other_free_text":[]}},"prefetch_data":{"uniprot":{"accession":"Q86UD0","full_name":"Suppressor APC domain-containing protein 2","aliases":["Tumor specificity and mitosis phase-dependent expression protein","TS/MDEP","p42.3"],"length_aa":394,"mass_kda":42.6,"function":"Plays a role in planar mitotic spindle orientation in retinal progenitor cells (RPCs) and promotes the production of symmetric terminal divisions (By similarity). Negatively regulates the mitotic apical cortex localization of GPSM2 (PubMed:26766442). Involved also in positive regulation of cell proliferation and tumor cell growth (PubMed:23576022, PubMed:23704824)","subcellular_location":"Cytoplasm; Nucleus; Cytoplasm, cell cortex; Apical cell membrane; Cell junction, tight junction","url":"https://www.uniprot.org/uniprotkb/Q86UD0/entry"},"depmap":{"release":"DepMap","has_data":true,"is_common_essential":false,"resolved_as":"","url":"https://depmap.org/portal/gene/SAPCD2","classification":"Not Classified","n_dependent_lines":4,"n_total_lines":1208,"dependency_fraction":0.0033112582781456954},"opencell":{"profiled":false,"resolved_as":"","ensg_id":"","cell_line_id":"","localizations":[],"interactors":[],"url":"https://opencell.sf.czbiohub.org/search/SAPCD2","total_profiled":1310},"omim":[{"mim_id":"612057","title":"SUPPRESSOR APC DOMAIN-CONTAINING PROTEIN 2; SAPCD2","url":"https://www.omim.org/entry/612057"}],"hpa":{"profiled":true,"resolved_as":"","reliability":"Supported","locations":[{"location":"Cytosol","reliability":"Supported"},{"location":"Nucleoplasm","reliability":"Additional"},{"location":"Nucleoli","reliability":"Additional"}],"tissue_specificity":"Tissue enhanced","tissue_distribution":"Detected in many","driving_tissues":[{"tissue":"brain","ntpm":12.8},{"tissue":"esophagus","ntpm":8.2}],"url":"https://www.proteinatlas.org/search/SAPCD2"},"hgnc":{"alias_symbol":["p42.3"],"prev_symbol":["C9orf140"]},"alphafold":{"accession":"Q86UD0","domains":[{"cath_id":"1.10.238,1.10.238","chopping":"27-98","consensus_level":"medium","plddt":84.6775,"start":27,"end":98}],"viewer_url":"https://alphafold.ebi.ac.uk/entry/Q86UD0","model_url":"https://alphafold.ebi.ac.uk/files/AF-Q86UD0-F1-model_v6.cif","pae_url":"https://alphafold.ebi.ac.uk/files/AF-Q86UD0-F1-predicted_aligned_error_v6.png","plddt_mean":67.94},"mouse_models":{"mgi_url":"https://www.informatics.jax.org/marker/summary?nomen=SAPCD2","jax_strain_url":"https://www.jax.org/strain/search?query=SAPCD2"},"sequence":{"accession":"Q86UD0","fasta_url":"https://rest.uniprot.org/uniprotkb/Q86UD0.fasta","uniprot_url":"https://www.uniprot.org/uniprotkb/Q86UD0/entry","alphafold_viewer_url":"https://alphafold.ebi.ac.uk/entry/Q86UD0"}},"corpus_meta":[{"pmid":"21998710","id":"PMC_21998710","title":"MiR-29a inhibits cell proliferation and induces cell cycle arrest through the downregulation of p42.3 in human gastric cancer.","date":"2011","source":"PloS one","url":"https://pubmed.ncbi.nlm.nih.gov/21998710","citation_count":89,"is_preprint":false},{"pmid":"17525738","id":"PMC_17525738","title":"Identification and characterization of a novel p42.3 gene as tumor-specific and mitosis phase-dependent expression in gastric cancer.","date":"2007","source":"Oncogene","url":"https://pubmed.ncbi.nlm.nih.gov/17525738","citation_count":38,"is_preprint":false},{"pmid":"26766442","id":"PMC_26766442","title":"SAPCD2 Controls Spindle Orientation and Asymmetric Divisions by Negatively Regulating the Gαi-LGN-NuMA Ternary Complex.","date":"2016","source":"Developmental cell","url":"https://pubmed.ncbi.nlm.nih.gov/26766442","citation_count":32,"is_preprint":false},{"pmid":"31173488","id":"PMC_31173488","title":"Long noncoding RNA PXN-AS1-L promotes the malignancy of nasopharyngeal carcinoma cells via upregulation of SAPCD2.","date":"2019","source":"Cancer medicine","url":"https://pubmed.ncbi.nlm.nih.gov/31173488","citation_count":24,"is_preprint":false},{"pmid":"33683171","id":"PMC_33683171","title":"YY1-inudced activation of lncRNA DUXAP8 promotes proliferation and suppresses apoptosis of triple negative breast cancer cells through upregulating SAPCD2.","date":"2021","source":"Cancer biology & therapy","url":"https://pubmed.ncbi.nlm.nih.gov/33683171","citation_count":23,"is_preprint":false},{"pmid":"29531269","id":"PMC_29531269","title":"C9orf140, a novel Axin1-interacting protein, mediates the negative feedback loop of Wnt/β-catenin signaling.","date":"2018","source":"Oncogene","url":"https://pubmed.ncbi.nlm.nih.gov/29531269","citation_count":17,"is_preprint":false},{"pmid":"23192843","id":"PMC_23192843","title":"Cell cycle-dependent expression of p42.3 promotes mitotic progression in malignant transformed cells.","date":"2012","source":"Molecular 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immunotherapeutics","url":"https://pubmed.ncbi.nlm.nih.gov/24051432","citation_count":12,"is_preprint":false},{"pmid":"35467005","id":"PMC_35467005","title":"MiR-486-5p specifically suppresses SAPCD2 expression, which attenuates the aggressive phenotypes of lung adenocarcinoma cells.","date":"2022","source":"Histology and histopathology","url":"https://pubmed.ncbi.nlm.nih.gov/35467005","citation_count":11,"is_preprint":false},{"pmid":"33384953","id":"PMC_33384953","title":"Silencing SAPCD2 Represses Proliferation and Lung Metastasis of Fibrosarcoma by Activating Hippo Signaling Pathway.","date":"2020","source":"Frontiers in oncology","url":"https://pubmed.ncbi.nlm.nih.gov/33384953","citation_count":10,"is_preprint":false},{"pmid":"28093638","id":"PMC_28093638","title":"Depletion of p42.3 gene inhibits proliferation and invasion in melanoma cells.","date":"2017","source":"Journal of cancer research and clinical 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Corroboration of the Regulatory Pathway of p42.3 Protein in the Pathogenesis of Gastric Carcinoma.","date":"2015","source":"Computational and mathematical methods in medicine","url":"https://pubmed.ncbi.nlm.nih.gov/26106439","citation_count":5,"is_preprint":false},{"pmid":"32793664","id":"PMC_32793664","title":"Expression of p42.3 in non-small cell lung cancer.","date":"2020","source":"Annals of translational medicine","url":"https://pubmed.ncbi.nlm.nih.gov/32793664","citation_count":4,"is_preprint":false},{"pmid":"27449033","id":"PMC_27449033","title":"Overexpression of p42.3 promotes cell proliferation, migration, and invasion in human gastric cancer cells.","date":"2016","source":"Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine","url":"https://pubmed.ncbi.nlm.nih.gov/27449033","citation_count":4,"is_preprint":false},{"pmid":"35517423","id":"PMC_35517423","title":"The Function and Regulation of SAPCD2 in Physiological and Oncogenic 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action of gastric carcinoma protein p42.3.","date":"2016","source":"Journal of cancer research and therapeutics","url":"https://pubmed.ncbi.nlm.nih.gov/28054541","citation_count":0,"is_preprint":false}],"cost":{"stage1":{"model":"claude-sonnet-4-6","input_tokens":16890,"output_tokens":3365,"usd":0.050572,"stage1_stop_reason":"end_turn"},"stage2":{"model":"claude-opus-4-8","input_tokens":10936,"output_tokens":2639,"usd":0.060327,"stage2_stop_reason":"end_turn"},"total_usd":0.110899,"stage1_batch_id":"msgbatch_013LWZZT6MWaqB9qyTSeQBmU","stage2_batch_id":"msgbatch_0194ZzQaTGNpruoNJBbEMbt3","note":"batch pricing = 50% of standard"},"stage1_raw":"```json\n{\n  \"discoveries\": [\n    {\n      \"year\": 2016,\n      \"finding\": \"SAPCD2 (p42.3) physically interacts with LGN and negatively regulates LGN localization at the cell cortex, likely by competing with NuMA for LGN binding, thereby controlling mitotic spindle orientation in epithelial cells and mouse retinal progenitor cells in vivo.\",\n      \"method\": \"Co-IP/pulldown to identify LGN as binding partner; siRNA loss-of-function in epithelial cyst cultures and in vivo retinal progenitor assays; competition binding assays with NuMA\",\n      \"journal\": \"Developmental cell\",\n      \"confidence\": \"High\",\n      \"confidence_rationale\": \"Tier 2 / Strong — reciprocal binding assays, clean KO/KD with defined cellular and in vivo phenotypes (spindle misorientation, cyst morphogenesis defects, tripled asymmetric divisions), multiple orthogonal methods across cell culture and animal model\",\n      \"pmids\": [\"26766442\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2026,\n      \"finding\": \"SAPCD2 functions as a microtubule-associated protein that promotes microtubule stability; CDK1-mediated phosphorylation at S157, together with phosphorylation at S276, generates a mitosis-specific isoform that destabilizes astral microtubules to control spindle orientation. Disruption of phosphorylation at both S157 and S276 fails to rescue spindle misorientation caused by SAPCD2 depletion.\",\n      \"method\": \"Live-cell imaging; siRNA depletion; phospho-site mutagenesis (S157A, S276A); microtubule stability assays; identification of CDK1 as the kinase for S157\",\n      \"journal\": \"Communications biology\",\n      \"confidence\": \"High\",\n      \"confidence_rationale\": \"Tier 1–2 / Moderate — phospho-site mutagenesis combined with live-cell imaging, in vitro kinase identification (CDK1), and functional rescue experiments in a single rigorous study\",\n      \"pmids\": [\"42151476\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2018,\n      \"finding\": \"C9orf140 (SAPCD2) is a negative regulator of Wnt/β-catenin signaling that interacts with Axin1, outcompetes PP2A for Axin1 binding, thereby shifting the balance toward phosphorylation of β-catenin and reducing Wnt3A-induced β-catenin accumulation. Wnt signaling in turn induces C9orf140 expression via β-catenin, forming a negative feedback loop.\",\n      \"method\": \"Tandem-affinity purification and mass spectrometry to identify Axin1 as binding partner; Co-IP; competition assay with PP2A; β-catenin phosphorylation assays in cultured cells; zebrafish embryo functional validation\",\n      \"journal\": \"Oncogene\",\n      \"confidence\": \"High\",\n      \"confidence_rationale\": \"Tier 1–2 / Strong — TAP-MS identification of binding partner, Co-IP, competition binding, functional phosphorylation assays, and in vivo zebrafish epistasis in a single study with multiple orthogonal methods\",\n      \"pmids\": [\"29531269\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2007,\n      \"finding\": \"p42.3 (SAPCD2) expression is cell cycle-dependent in gastric cancer cell lines, with peak expression at M phase. RNAi-mediated depletion causes G2/M arrest, suppresses cell proliferation and tumorigenicity, and alters expression of cyclin B1 and Chk2.\",\n      \"method\": \"Cell cycle synchronization + RT-PCR/Western blot; siRNA knockdown; colony formation and xenograft tumorigenicity assays; flow cytometry\",\n      \"journal\": \"Oncogene\",\n      \"confidence\": \"Medium\",\n      \"confidence_rationale\": \"Tier 2 / Moderate — clean KD with defined cell cycle phenotype and downstream marker changes, single lab, two orthogonal functional assays\",\n      \"pmids\": [\"17525738\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2012,\n      \"finding\": \"p42.3 (SAPCD2) overexpression in NIH3T3 cells promotes malignant transformation with accelerated mitotic progression, altered chromosome segregation, upregulation of Cyclin B1, and downregulation of Cdc2-Tyr15 phosphorylation.\",\n      \"method\": \"Stable transfection of p42.3 into NIH3T3 cells; Western blot for cell cycle proteins; mitotic progression assays\",\n      \"journal\": \"Molecular carcinogenesis\",\n      \"confidence\": \"Medium\",\n      \"confidence_rationale\": \"Tier 2 / Moderate — gain-of-function with defined molecular readouts (Cyclin B1, Cdc2-Tyr15), single lab, multiple assay types\",\n      \"pmids\": [\"23192843\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2022,\n      \"finding\": \"SAPCD2 directly binds cytoplasmic E2F7 (but not E2F1) and alters its subcellular distribution; SAPCD2 knockdown increases nuclear E2F7 accumulation, thereby affecting expression of genes involved in cell cycle regulation and chromosome instability in neuroblastoma cells.\",\n      \"method\": \"Co-IP to demonstrate direct SAPCD2–E2F7 (not E2F1) binding; subcellular fractionation; siRNA knockdown with gene expression profiling; in vitro and in vivo functional assays\",\n      \"journal\": \"Cell death & disease\",\n      \"confidence\": \"Medium\",\n      \"confidence_rationale\": \"Tier 2 / Moderate — Co-IP binding assay, subcellular fractionation showing redistribution of E2F7, KD phenotype with pathway-level readout, single lab\",\n      \"pmids\": [\"35197448\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2011,\n      \"finding\": \"miR-29a directly binds the 3′UTR of p42.3 (SAPCD2) mRNA to repress p42.3 expression at both mRNA and protein levels, inducing cell cycle arrest and inhibiting proliferation in gastric cancer cells.\",\n      \"method\": \"3′UTR luciferase reporter assay; Western blot and qRT-PCR; miR-29a mimic transfection; cell cycle analysis\",\n      \"journal\": \"PloS one\",\n      \"confidence\": \"Medium\",\n      \"confidence_rationale\": \"Tier 2 / Moderate — direct 3′UTR reporter validation of miRNA-mRNA interaction, functional cell cycle readout, single lab\",\n      \"pmids\": [\"21998710\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2020,\n      \"finding\": \"Silencing SAPCD2 in fibrosarcoma cells activates the Hippo signaling pathway (reduces YAP1 activity); constitutively active YAP1-S127A rescues the inhibitory effects of SAPCD2 knockdown on colony formation, anchorage-independent growth, and apoptosis, placing SAPCD2 upstream of YAP1 in this pathway.\",\n      \"method\": \"siRNA knockdown; genetic epistasis with YAP1-S127A rescue construct; colony formation and anchorage-independent growth assays; apoptosis assay; in vivo lung metastasis model\",\n      \"journal\": \"Frontiers in oncology\",\n      \"confidence\": \"Medium\",\n      \"confidence_rationale\": \"Tier 2 / Moderate — genetic epistasis (YAP1-S127A rescue) establishes pathway position, complemented by in vivo model, single lab\",\n      \"pmids\": [\"33384953\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2020,\n      \"finding\": \"SAPCD2 knockdown in breast cancer cells reduces YAP/TAZ protein expression and inhibits proliferation, migration, and invasion; simultaneous YAP overexpression reverses these effects, placing SAPCD2 upstream of YAP/TAZ.\",\n      \"method\": \"siRNA knockdown; YAP overexpression rescue; Western blot for YAP/TAZ; CCK-8, transwell assays\",\n      \"journal\": \"European review for medical and pharmacological sciences\",\n      \"confidence\": \"Low\",\n      \"confidence_rationale\": \"Tier 3 / Weak — single lab, rescue experiment shows epistatic relationship but mechanistic link between SAPCD2 and YAP/TAZ is not biochemically characterized\",\n      \"pmids\": [\"32329855\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2019,\n      \"finding\": \"LncRNA PXN-AS1-L directly interacts with SAPCD2 mRNA 3′UTR to prevent miRNA-AGO silencing complex binding, thereby upregulating SAPCD2 mRNA and protein levels in nasopharyngeal carcinoma cells.\",\n      \"method\": \"RNA pull-down / RNA-RNA interaction assay; qRT-PCR and Western blot; SAPCD2 depletion rescue experiments in vitro and in vivo\",\n      \"journal\": \"Cancer medicine\",\n      \"confidence\": \"Low\",\n      \"confidence_rationale\": \"Tier 3 / Weak — RNA-RNA interaction proposed and supported by pulldown, but AGO competition mechanism not biochemically reconstituted; single lab\",\n      \"pmids\": [\"31173488\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2026,\n      \"finding\": \"SAPCD2 stabilizes TANK protein by preventing its ubiquitin-mediated degradation by SYVN1, activates MAPK signaling, and through CREB phosphorylation enhances PLAGL2 expression, which in turn amplifies SAPCD2 expression in a positive feedback loop driving bladder cancer progression.\",\n      \"method\": \"Co-IP; ubiquitination assays; CREB phosphorylation assays; siRNA/overexpression functional assays; in vivo tumor models\",\n      \"journal\": \"Cancers\",\n      \"confidence\": \"Low\",\n      \"confidence_rationale\": \"Tier 3 / Weak — mechanistic claims from a single lab with Co-IP and phosphorylation assays, but abstract provides limited methodological detail on reconstitution or mutagenesis\",\n      \"pmids\": [\"41682005\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2014,\n      \"finding\": \"STAT5 directly interacts with EZH2 and β-catenin to enhance C9orf140 (SAPCD2) gene transactivation, and C9orf140 promotes epithelial-mesenchymal transition and CRC cell invasion downstream of STAT5, EZH2, and β-catenin.\",\n      \"method\": \"siRNA knockdown and overexpression; Co-IP for STAT5-EZH2-β-catenin interaction; EMT marker analysis; in vivo metastasis model\",\n      \"journal\": \"Carcinogenesis\",\n      \"confidence\": \"Low\",\n      \"confidence_rationale\": \"Tier 3 / Weak — Co-IP for upstream complex, KD/OE with pathway readout, single lab, mechanistic details limited in abstract\",\n      \"pmids\": [\"24608043\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2023,\n      \"finding\": \"SAPCD2 protein is localized predominantly in the cytoplasm of CRC cells, as determined by immunofluorescence with SAPCD2-EGFP recombinant constructs.\",\n      \"method\": \"Immunofluorescence with SAPCD2-EGFP fusion constructs in HCT116 cells\",\n      \"journal\": \"Cellular and molecular biology\",\n      \"confidence\": \"Low\",\n      \"confidence_rationale\": \"Tier 3 / Weak — direct localization by fluorescent construct, single lab, no functional consequence linked to localization\",\n      \"pmids\": [\"38158695\"],\n      \"is_preprint\": false\n    }\n  ],\n  \"current_model\": \"SAPCD2 (p42.3/C9orf140) is a cell cycle-regulated protein that functions as a microtubule-associated protein controlling astral microtubule stability and mitotic spindle orientation: its activity is toggled by CDK1-mediated phosphorylation at S157 (and S276), creating a mitosis-specific isoform that destabilizes astral microtubules; it also directly binds LGN and competes with NuMA to limit cortical LGN accumulation, thereby restraining planar spindle orientation during epithelial morphogenesis and asymmetric cell division; additionally, SAPCD2 interacts with Axin1 to outcompete PP2A, shifting β-catenin toward phosphorylation and acting as a negative feedback regulator of Wnt/β-catenin signaling; in cancer contexts it binds cytoplasmic E2F7 to restrict its nuclear accumulation, activates YAP/TAZ and Hippo pathway components, and stabilizes TANK to sustain MAPK signaling, while its own expression is post-transcriptionally regulated by miR-29a and miR-486-5p via 3′UTR binding.\"\n}\n```","stage2_raw":"{\n  \"mechanistic_narrative\": \"SAPCD2 (p42.3/C9orf140) is a cell cycle-regulated, cytoplasmic protein that controls mitotic spindle orientation by acting as a microtubule-associated protein [#1, #3]. It directly binds LGN and negatively regulates LGN accumulation at the cell cortex, competing with NuMA to limit cortical LGN and thereby restraining planar spindle orientation during epithelial morphogenesis and asymmetric division of retinal progenitors [#0]. CDK1-mediated phosphorylation at S157, together with phosphorylation at S276, generates a mitosis-specific isoform that destabilizes astral microtubules; disruption of both sites prevents rescue of the spindle misorientation caused by SAPCD2 loss [#1]. Independently, SAPCD2 acts as a negative-feedback regulator of Wnt/\\u03b2-catenin signaling by binding Axin1 and outcompeting PP2A, shifting \\u03b2-catenin toward phosphorylation, while Wnt signaling itself induces SAPCD2 expression [#2]. In cancer contexts SAPCD2 drives proliferation and tumorigenicity, with expression peaking at M phase and depletion causing G2/M arrest [#3]; it directly binds cytoplasmic E2F7 to restrict its nuclear accumulation [#5] and operates upstream of YAP1 to regulate Hippo-pathway-dependent growth [#7]. Its expression is post-transcriptionally repressed by miR-29a binding the 3\\u2032UTR [#6].\",\n  \"teleology\": [\n    {\n      \"year\": 2007,\n      \"claim\": \"Established SAPCD2 (p42.3) as a cell cycle-dependent, proliferation-promoting protein, defining its first functional context before any molecular mechanism was known.\",\n      \"evidence\": \"Cell cycle synchronization with RT-PCR/Western, siRNA knockdown, colony formation and xenograft assays in gastric cancer cells\",\n      \"pmids\": [\"17525738\"],\n      \"confidence\": \"Medium\",\n      \"gaps\": [\"No molecular partner or biochemical activity identified\", \"Mechanism linking SAPCD2 to cyclin B1/Chk2 changes unresolved\"]\n    },\n    {\n      \"year\": 2011,\n      \"claim\": \"Identified an upstream regulatory input by showing miR-29a directly represses SAPCD2 via its 3\\u2032UTR, placing SAPCD2 within a defined post-transcriptional control axis.\",\n      \"evidence\": \"3\\u2032UTR luciferase reporter, miR-29a mimic, Western/qRT-PCR and cell cycle analysis in gastric cancer cells\",\n      \"pmids\": [\"21998710\"],\n      \"confidence\": \"Medium\",\n      \"gaps\": [\"Does not address downstream effector function of SAPCD2\", \"Only one regulatory miRNA tested\"]\n    },\n    {\n      \"year\": 2012,\n      \"claim\": \"Demonstrated SAPCD2 is oncogenic gain-of-function, accelerating mitotic progression and altering chromosome segregation, reinforcing a mitotic role.\",\n      \"evidence\": \"Stable overexpression in NIH3T3 cells with cell cycle protein Western blots and mitotic progression assays\",\n      \"pmids\": [\"23192843\"],\n      \"confidence\": \"Medium\",\n      \"gaps\": [\"No direct molecular target of SAPCD2 identified\", \"Mechanism of altered segregation not defined\"]\n    },\n    {\n      \"year\": 2016,\n      \"claim\": \"Provided the first direct molecular mechanism: SAPCD2 binds LGN and competes with NuMA to limit cortical LGN, controlling spindle orientation and asymmetric division in vivo.\",\n      \"evidence\": \"Co-IP/pulldown, NuMA competition assays, siRNA in epithelial cysts and mouse retinal progenitors\",\n      \"pmids\": [\"26766442\"],\n      \"confidence\": \"High\",\n      \"gaps\": [\"Structural basis of LGN binding not resolved\", \"Did not establish how SAPCD2 itself is recruited to the cortex\"]\n    },\n    {\n      \"year\": 2018,\n      \"claim\": \"Revealed a distinct signaling function as a negative-feedback regulator of Wnt/\\u03b2-catenin through Axin1 binding and PP2A competition.\",\n      \"evidence\": \"TAP-MS, Co-IP, PP2A competition, \\u03b2-catenin phosphorylation assays, zebrafish epistasis\",\n      \"pmids\": [\"29531269\"],\n      \"confidence\": \"High\",\n      \"gaps\": [\"Relationship between Wnt-regulatory and spindle-orientation functions unclear\", \"No structural detail of the Axin1 interaction\"]\n    },\n    {\n      \"year\": 2022,\n      \"claim\": \"Showed SAPCD2 directly binds cytoplasmic E2F7 and restricts its nuclear accumulation, linking SAPCD2 to transcriptional control of cell cycle and chromosome stability genes.\",\n      \"evidence\": \"Co-IP (E2F7-specific, not E2F1), subcellular fractionation, siRNA with expression profiling in neuroblastoma\",\n      \"pmids\": [\"35197448\"],\n      \"confidence\": \"Medium\",\n      \"gaps\": [\"Mechanism of cytoplasmic sequestration not defined\", \"Reciprocal validation of binding limited\"]\n    },\n    {\n      \"year\": 2026,\n      \"claim\": \"Defined the mitotic switch mechanism: CDK1 phosphorylates SAPCD2 at S157 (with S276) to create a microtubule-destabilizing, mitosis-specific isoform required for correct spindle orientation.\",\n      \"evidence\": \"Live-cell imaging, phospho-site mutagenesis (S157A, S276A), in vitro CDK1 kinase identification, rescue experiments\",\n      \"pmids\": [\"42151476\"],\n      \"confidence\": \"High\",\n      \"gaps\": [\"Structural basis of microtubule binding unresolved\", \"How phosphorylation alters microtubule association mechanistically not shown\"]\n    },\n    {\n      \"year\": null,\n      \"claim\": \"It remains unclear how SAPCD2's distinct activities — astral microtubule destabilization, cortical LGN competition, Wnt/Axin1 feedback, and E2F7/YAP regulation — are integrated within a single cell or coordinated across cell-cycle stages.\",\n      \"evidence\": \"No single study reconciles the spindle-orientation and signaling roles\",\n      \"pmids\": [],\n      \"confidence\": \"Low\",\n      \"gaps\": [\"No structural model of SAPCD2\", \"No unified framework connecting its microtubule and signaling functions\", \"Domain architecture mediating the multiple interactions undefined\"]\n    }\n  ],\n  \"mechanism_profile\": {\n    \"molecular_activity\": [\n      {\"term_id\": \"GO:0008092\", \"supporting_discovery_ids\": [1]},\n      {\"term_id\": \"GO:0098772\", \"supporting_discovery_ids\": [0, 2]}\n    ],\n    \"localization\": [\n      {\"term_id\": \"GO:0005829\", \"supporting_discovery_ids\": [12, 5]},\n      {\"term_id\": \"GO:0005856\", \"supporting_discovery_ids\": [1]}\n    ],\n    \"pathway\": [\n      {\"term_id\": \"R-HSA-1640170\", \"supporting_discovery_ids\": [1, 3]},\n      {\"term_id\": \"R-HSA-162582\", \"supporting_discovery_ids\": [2]}\n    ],\n    \"complexes\": [],\n    \"partners\": [\"LGN\", \"NuMA\", \"Axin1\", \"PP2A\", \"E2F7\"],\n    \"other_free_text\": []\n  }\n}","audit_flag":null,"evaluation":{"pairwise":"win","faith_supported":5,"faith_total":6,"faith_pct":83.33333333333333}}