Affinage

SEMA3C

Semaphorin-3C · UniProt Q99985

Length
751 aa
Mass
85.2 kDa
Annotated
2026-04-28
36 papers in source corpus 22 papers cited in narrative 22 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

SEMA3C is a secreted class 3 semaphorin that acts as an autocrine and paracrine signaling ligand through context-dependent engagement of neuropilin (NRP1, NRP2) and plexin (PlexinA2, PlexinB1, PlexinD1) co-receptor complexes, as well as ITGB1, to activate Rac1/NF-κB, Wnt/β-catenin, MAPK, AKT, and Hedgehog signaling cascades (PMID:25464848, PMID:37080989, PMID:29348142, PMID:38956074, PMID:34742786). In development, neural crest–derived SEMA3C activates NRP1-dependent endothelial-to-mesenchymal transition required for cardiac outflow tract septation, regulates cortical neuron polarity and radial migration downstream of Bcl11a-mediated transcriptional repression, and modulates motor axon guidance by differentially controlling NRP1/NRP2 surface levels at growth cones (PMID:26053665, PMID:26182416, PMID:22899844). SEMA3C transcription is directly controlled by multiple transcription factors—repressed by Bcl11a and FOXA1, and activated by Foxc1/c2, FOXM1, Twist1, KLF6/FOSL2/p300, and a LINE-1 enhancer/BRD4 condensate axis—enabling tissue- and disease-specific expression (PMID:26182416, PMID:38528115, PMID:28754980, PMID:34742786, PMID:33420365, PMID:40082673, PMID:41984404). In cancer, SEMA3C sustains glioma and breast cancer stem cell survival via Rac1-dependent β-catenin nuclear accumulation and Wnt target gene activation, and drives ligand-independent transactivation of EGFR, ErbB2, and MET through PlexinB1 (PMID:37080989, PMID:25464848, PMID:29348142, PMID:41984404).

Mechanistic history

Synthesis pass · year-by-year structured walk · 12 steps
  1. 2012 Medium

    Establishing that SEMA3C acts cell-autonomously in motor neurons to tune growth cone responsiveness by reciprocally modulating NRP1 and NRP2 surface levels, thereby determining motor nerve trajectory—revealing SEMA3C as an intrinsic regulator of semaphorin sensitivity, not merely an extrinsic cue.

    Evidence Targeted gain/loss-of-function in chick neural tube with growth cone surface receptor quantification and in vivo nerve trajectory analysis

    PMID:22899844

    Open questions at the time
    • Single-lab study in chick; not replicated in mammalian model
    • Downstream signaling mediating NRP surface level changes undefined
    • Whether this mechanism operates in sensory or other axon types unknown
  2. 2014 High

    Demonstrating that SEMA3C functions as an autocrine survival factor for glioma stem cells through PlexinA2/D1 receptors and Rac1/NF-κB signaling—the first identification of a semaphorin autocrine loop in brain tumor maintenance, with Rac1 placed epistatically downstream.

    Evidence Knockdown in orthotopic glioblastoma models, receptor co-expression analysis, Rac1 constitutive-active rescue in vivo

    PMID:25464848

    Open questions at the time
    • Direct physical interaction between SEMA3C and PlexinA2/D1 not shown by binding assay
    • Mechanism linking receptor activation to Rac1 unclear
    • Whether NRP co-receptors participate in GSC context not tested
  3. 2015 High

    Defining SEMA3C as a critical effector in two distinct developmental programs—cortical neuron migration (repressed by Bcl11a) and cardiac outflow tract septation (activating EndMT via NRP1)—establishing its dual developmental significance.

    Evidence ChIP for Bcl11a at Sema3c promoter, conditional knockout mice with in vivo rescue (cortex); ligand/tissue-specific mutants, lineage tracing, explant assays (heart)

    PMID:26053665 PMID:26182416

    Open questions at the time
    • Downstream intracellular signaling mediating EndMT in outflow tract not fully resolved
    • Whether Bcl11a-SEMA3C axis operates outside upper-layer neurons untested
    • Identity of the SEMA3C receptor complex in cortical migration not defined
  4. 2017 Medium

    Revealing that SEMA3C transcription in the outflow tract is positively controlled by Foxc1/c2 and negatively regulated by Tbx1-driven Fgf8/ERK signaling in cardiac neural crest cells—providing the upstream transcriptional logic for spatially restricted SEMA3C expression during heart development.

    Evidence Promoter reporter assays, ChIP for Foxc1/c2, FGF8 blocking experiments in chick with ERK readout

    PMID:28754980

    Open questions at the time
    • Single-lab study
    • Whether Foxc1/c2 and Fgf8/ERK converge on the same promoter elements unknown
    • Mammalian validation of FGF8-ERK repression incomplete
  5. 2018 High

    Identifying PlexinB1 as the receptor through which SEMA3C transactivates RTKs (EGFR, ErbB2, MET) in a cognate ligand-independent manner, and demonstrating that Ephrin-B1 silences SEMA3C/NRP1 attraction in commissural axons via direct glycosylation-dependent NRP1 binding—together resolving two distinct receptor-level regulatory mechanisms.

    Evidence Co-IP/pulldown and PlexinB1-Fc fusion inhibition in xenograft (prostate cancer); Co-IP of Ephrin-B1–NRP1, N-glycosylation mutagenesis, in vivo axon guidance assays (corpus callosum)

    PMID:29348142 PMID:29779877

    Open questions at the time
    • Structural basis of PlexinB1-mediated RTK transactivation unknown
    • Whether Ephrin-B1 silencing mechanism applies to non-callosal axon systems untested
    • Furin cleavage requirement for RTK transactivation not addressed
  6. 2018 Medium

    Establishing that furin processing at the 742RNRR745 basic domain cleavage site is required for SEMA3C anti-angiogenic activity, indicating post-translational processing regulates functional output.

    Evidence Site-directed mutagenesis of furin site (R745A), HUVEC tube formation assay

    PMID:30304095

    Open questions at the time
    • Single-lab, in vitro only
    • Whether furin cleavage regulates SEMA3C activities beyond angiogenesis unknown
    • No in vivo validation
  7. 2019 Medium

    Demonstrating NRP2-selective signaling for SEMA3C in corneal epithelium, where it promotes wound healing and sensory nerve regeneration—showing that receptor choice (NRP2 vs. NRP1) dictates tissue-specific outcomes.

    Evidence siRNA knockdown, NRP2 neutralizing antibodies, exogenous SEMA3C in diabetic cornea model in vivo

    PMID:30679185

    Open questions at the time
    • Downstream intracellular signaling in corneal cells not defined
    • Single-lab study
    • Whether PlexinD1 participates as a co-receptor in cornea untested
  8. 2021 Medium

    Expanding the transcriptional regulation network: MAOA/Twist1 directly activates SEMA3C to drive cMET-mediated perineural invasion; FOXM1 activates SEMA3C to induce NRP2/Hedgehog-dependent M2 macrophage polarization; and the lncRNA LETR1 epigenetically maintains SEMA3C in lymphatic endothelial cells—demonstrating pervasive transcriptional control across tissues.

    Evidence ChIP for Twist1 and FOXM1 at SEMA3C promoter, SMO antagonist epistasis, lncRNA knockdown/rescue, in vivo models (pancreatic cancer, wound healing, lymphatics)

    PMID:33420365 PMID:33568674 PMID:34742786

    Open questions at the time
    • How LETR1 mechanistically controls SEMA3C chromatin state undefined
    • Whether FOXM1-SEMA3C-Hedgehog axis operates outside wound context unknown
    • Twist1 binding specificity at SEMA3C promoter relative to other Twist1 targets not characterized
  9. 2023 High

    Resolving that SEMA3C drives Wnt-independent β-catenin nuclear accumulation via Rac1 in glioma stem cells, activating TCF/LEF targets—explaining how SEMA3C sustains stemness without canonical Wnt ligands and establishing combinatorial therapeutic vulnerability with TCF1.

    Evidence β-catenin localization assays, Rac1 dependency experiments, Wnt ligand secretion suppression, combinatorial depletion in mouse GBM model

    PMID:37080989

    Open questions at the time
    • How Rac1 mechanistically promotes β-catenin nuclear import unresolved
    • Whether this Wnt-independent mechanism operates in non-glioma stem cells unknown
    • Identity of critical TCF/LEF target genes downstream not defined
  10. 2024 Medium

    Identifying ITGB1 as an additional SEMA3C co-receptor (alongside NRP1) that mediates AKT/Gli1/c-Myc signaling for HCC self-renewal and NF-κB-dependent IL-6/cholesterol synthesis in hepatic stellate cells, and defining FOXA1 as a direct transcriptional repressor of SEMA3C through intronic elements whose cancer-associated mutations de-repress expression.

    Evidence Co-IP of SEMA3C–NRP1–ITGB1, receptor knockdown, in vivo tumor models (HCC); ChIP-seq and luciferase reporters with FOXA1 forkhead domain mutants (prostate cancer)

    PMID:38528115 PMID:38956074

    Open questions at the time
    • Whether ITGB1 directly contacts SEMA3C or is bridged by NRP1 unknown
    • FOXA1 intronic regulatory mechanism not structurally characterized
    • Single-lab studies for both findings
  11. 2025 Medium

    Revealing a LINE-1 retrotransposon-derived cis-enhancer within the Sema3c locus that forms BRD4/H3K27ac phase-separated condensates to drive SEMA3C transcription in breast cancer stem cells, and defining KLF6/FOSL2/p300-mediated H3K23 succinylation as an epigenetic activation mechanism in chemoresistant colon cancer—providing two novel chromatin-level regulatory paradigms.

    Evidence CRISPRa, dual-luciferase reporter, BRD4 PROTAC degradation, receptor knockdown (breast cancer); CUT&Tag, ATAC-seq, ChIP for KLF6/FOSL2, knockdown (colon cancer)

    PMID:40082673 PMID:41984404

    Open questions at the time
    • Whether LINE-1 enhancer mechanism is generalizable across SEMA3C-expressing tissues unknown
    • H3K23 succinylation role awaits independent confirmation
    • Single-lab studies
  12. 2025 Medium

    Extending SEMA3C receptor biology to NRP2/MAPK in colorectal cancer liver metastasis initiation (CAF-secreted) and to PlexinD1/NRP2 in astrocyte-mediated dendrite growth inhibition relevant to Rett syndrome pathology.

    Evidence Co-culture and in vivo metastasis models with SEMA3C–NRP2 binding (CRC); astrocyte-neuron co-culture, conditional genetic reduction in RTT mouse model with behavioral rescue (preprint)

    PMID:40402249 PMID:41279175

    Open questions at the time
    • RTT finding is a preprint, not yet peer-reviewed
    • Whether SEMA3C reduction is a viable therapeutic strategy for Rett syndrome untested clinically
    • Downstream MAPK effectors in liver metastasis initiation not identified

Open questions

Synthesis pass · forward-looking unresolved questions
  • Major open questions include: the structural basis for SEMA3C's engagement of distinct receptor complexes in different tissues; the mechanism by which Rac1 promotes β-catenin nuclear accumulation downstream of plexin/neuropilin activation; whether the multiple transcriptional regulators of SEMA3C operate through shared or independent chromatin domains; and the in vivo relevance of furin processing across SEMA3C's biological functions.
  • No structural model of SEMA3C–receptor complex exists
  • Rac1-to-β-catenin mechanism molecularly undefined
  • Integrated chromatin map of SEMA3C regulatory elements across cell types lacking

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0048018 receptor ligand activity 7 GO:0098772 molecular function regulator activity 2
Localization
GO:0005576 extracellular region 6
Pathway
R-HSA-162582 Signal Transduction 6 R-HSA-1266738 Developmental Biology 4 R-HSA-1643685 Disease 4
Partners
BRD4EFNB1ITGB1NRP1NRP2PLXNA2PLXNB1PLXND1

Evidence

Reading pass · 22 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2014 SEMA3C promotes glioma stem cell (GSC) survival through an autocrine/paracrine loop: GSCs preferentially secrete SEMA3C and co-express PlexinA2/D1 receptors, activating Rac1/NF-κB signaling. Introduction of activated Rac1 rescued the SEMA3C knockdown phenotype in vivo, placing SEMA3C upstream of Rac1 in this pathway. Knockdown in orthotopic glioblastoma models, receptor co-expression analysis, Rac1 rescue experiment in vivo Cell Reports High 25464848
2015 Bcl11a is a direct negative transcriptional regulator of Sema3C in cortical neurons; loss of Bcl11a increases Sema3C expression, and Sema3C elevation causes failure of multipolar-to-bipolar polarity switch and impaired radial migration of upper-layer cortical neurons. In vivo gain-of-function and rescue experiments confirmed Sema3C as the major downstream effector of Bcl11a. In vivo gain-of-function and rescue experiments, ChIP (direct binding of Bcl11a to Sema3C promoter), conditional knockout mice Neuron High 26182416
2015 Neural crest-derived SEMA3C activates NRP1 on outflow tract endothelium to promote endothelial-to-mesenchymal transition (EndMT), supplying cells to endocardial cushions and repositioning cardiac neural crest cells, both required for cardiac outflow tract septal bridge formation. Ligand-specific and tissue-specific mouse mutants, explant assays, gene-expression studies, lineage tracing Journal of Clinical Investigation High 26053665
2018 SEMA3C drives activation of multiple receptor tyrosine kinases (EGFR, ErbB2, MET) in a cognate ligand-independent manner via PlexinB1. Plexin B1 sema domain:Fc fusion proteins suppress RTK signaling and cell growth, and inhibit CRPC progression in vivo. Co-IP/pulldown, Plexin B1 Fc fusion inhibitor in vitro and in vivo xenograft model, RTK phosphorylation assays EMBO Molecular Medicine High 29348142
2018 Ephrin-B1 upregulation in post-crossing corpus callosum axons inhibits Sema3C/Neuropilin-1 signaling to silence the attractant response to Sema3C. This silencing is independent of Eph receptors and requires N-glycosylation at N-139 in the Ephrin-B1 extracellular domain, which mediates physical interaction with Nrp1. In vivo axon guidance assays, epistasis experiments, co-immunoprecipitation of Ephrin-B1 with Nrp1, N-glycosylation site mutagenesis Current Biology High 29779877
2017 Foxc1/c2 transcription factors directly activate Sema3C transcription in the outflow tract, while Tbx1-driven Fgf8 inhibits Sema3C expression in cardiac neural crest cells via ERK1/2 signaling. Blocking FGF8 causes ectopic SEMA3C expression and cNCC migration defects. Promoter reporter assays, ChIP, FGF8 blocking experiments in chick, ERK1/2 signaling readout Scientific Reports Medium 28754980
2021 MAOA promotes SEMA3C expression via Twist1-dependent transcriptional activation; SEMA3C in turn stimulates cMET to facilitate perineural invasion through autocrine/paracrine co-activation with PlexinA2 and NRP1 co-receptors. Knockdown/overexpression, co-culture PNI assay, in vivo orthotopic xenograft, signaling pathway analysis (cMET phosphorylation), ChIP for Twist1 on SEMA3C promoter Oncogene High 33420365
2023 Sema3C directs β-catenin nuclear accumulation in a Rac1-dependent process in glioma stem cells, leading to transcriptional activation of Wnt target genes independent of Wnt ligand binding. Combined depletion of Sema3C and TCF1 extended survival in a mouse glioblastoma model more than single inhibition. β-catenin localization assays, Rac1 dependency experiments, Wnt ligand secretion suppression, mouse glioblastoma model with combinatorial depletion Nature Communications High 37080989
2012 Motoneuronal Sema3C expression regulates surface levels of Nrp1 and Nrp2 at the growth cone in opposing ways, thereby modulating responsiveness to exogenous Sema3A, Sema3F, and Sema3C repellents and determining stereotyped motor nerve trajectory positioning in chick forelimb. Targeted gain- and loss-of-function in chick neural tube, growth cone surface receptor quantification, in vivo motor nerve trajectory analysis Development Medium 22899844
2018 The furin cleavage site 742RNRR745 in the basic domain of Sema3C is essential for its anti-angiogenic activity: point mutation R745A abrogates inhibition of microcapillary formation by human umbilical vein endothelial cells in vitro. Site-directed mutagenesis of furin cleavage site, in vitro angiogenesis assay (HUVEC tube formation) Brazilian Journal of Medical and Biological Research Medium 30304095
2024 SEMA3C binds NRP1 and ITGB1 receptors to activate AKT/Gli1/c-Myc signaling for HCC self-renewal. In hepatic stellate cells, SEMA3C interaction with NRP1 and ITGB1 activates NF-κB signaling, stimulating IL-6 release and HMGCR-mediated cholesterol synthesis. CAF-secreted TGF-β1 activates AP1 signaling to upregulate SEMA3C in HCC cells, forming a positive feedback loop. Co-IP (SEMA3C with NRP1 and ITGB1), signaling pathway analysis, in vivo tumor models, receptor knockdown Signal Transduction and Targeted Therapy Medium 38956074
2019 SEMA3C signals through NRP2 (not NRP1) in corneal epithelial cells to promote wound healing and sensory nerve regeneration. siRNA knockdown of SEMA3C or NRP2-neutralizing antibodies decreased wound healing and nerve regeneration; exogenous SEMA3C had opposing effects in diabetic corneas. NRP1 neutralization had a detrimental role in nerve regeneration. siRNA knockdown in vivo, NRP2 neutralizing antibodies, exogenous protein injection, wound healing assay, nerve fiber counting Diabetes Medium 30679185
2021 FOXM1 binds the promoter region of SEMA3C to directly elevate its expression; SEMA3C then upregulates NRP2 and activates Hedgehog signaling (SMO-dependent) to promote M2 macrophage polarization and fibroblast proliferation/migration in diabetic wound healing. ChIP (FOXM1 binding to SEMA3C promoter), knockdown/overexpression, SMO antagonist epistasis, M2 polarization assay, wound healing model Diabetes Research and Clinical Practice Medium 34742786
2021 The lncRNA LETR1 regulates SEMA3C expression in lymphatic endothelial cells as a nuclear trans-acting lncRNA via epigenetic factors; knockdown of LETR1 reduces SEMA3C levels and impairs LEC migratory ability, which is rescued by SEMA3C restoration. Antisense oligonucleotide knockdown, transcriptomic profiling, RNA-DNA and RNA-protein interaction studies, phenotype rescue assay Nature Communications Medium 33568674
2025 CAF-secreted SEMA3C binds NRP2 receptor on colorectal cancer liver metastasis-initiating cells, activating the MAPK pathway to promote liver metastasis. Co-culture experiments, receptor-ligand binding (SEMA3C-NRP2), in vivo and in vitro functional assays, MAPK pathway activation readout PNAS Medium 40402249
2021 SEMA3C overexpression in LNCaP prostate cancer cells promotes androgen synthesis in prostatic stromal cells through paracrine induction of Sonic Hedgehog (Shh) signaling (not direct SEMA3C action), as blocking Shh with a smoothened antagonist negated the steroidogenic effect. Conditioned media treatment, liquid chromatography-mass spectrometry for androgen quantification, SMO antagonist epistasis, qPCR for steroidogenic enzymes The Prostate Medium 33503318
2024 FOXA1 directly and negatively regulates SEMA3C transcription via intronic cis elements; FOXA1 forkhead domain mutations attenuate this inhibitory function (shown in reporter assays), leading to elevated SEMA3C levels in prostate cancer. Luciferase reporter assays, ChIP-seq analysis, analysis of prostate cancer specimens with FOXA1 mutations Scientific Reports Medium 38528115
2025 SEMA3C inhibits dendrite outgrowth in cortical neurons via PLXND1 and NRP2 receptors. Genetic reduction of astrocyte-secreted SEMA3C in female Rett Syndrome model mice enhances dendritic arborization, normalizes synaptic activity, visual acuity, and motor behavior. Astrocyte-neuron co-culture, receptor knockdown (PLXND1, NRP2), conditional genetic reduction in RTT mouse model, electrophysiology, behavioral assays bioRxiv (preprint)preprint Medium 41279175
2025 A LINE-1 retrotransposon within Sema3c (Sema3c_L1Md_T) acts as a cis-regulatory enhancer, forming phase-separated nuclear condensates with BRD4 at H3K27ac-marked regions to drive SEMA3C transcription. SEMA3C sustains breast cancer stem cell survival via NRP1, PlexinA2, and PlexinD1 receptors. BRD4 PROTAC degradation reduces SEMA3C levels and decreases BCSC viability. Dual-luciferase reporter assay, CRISPRa (dCas9-based), RNA-seq, ChIP, BRD4 PROTAC treatment, receptor knockdown (NRP1, PlexinA2, PlexinD1), in vivo tumor models Science China Life Sciences Medium 41984404
2025 MALAT1 positively regulates SEMA3C expression in intracranial aneurysm vascular smooth muscle cells; SEMA3C mediates downstream Smad pathway activation, promoting VSMC phenotype switching from contractile to synthetic type and inflammatory cytokine release. SEMA3C overexpression reverses the effects of MALAT1 silencing. Lentiviral overexpression/knockdown, epistasis (SEMA3C OE reverting MALAT1 KD phenotype), Smad pathway activation assay, in vivo IA rat model Frontiers in Cellular Neuroscience Medium 41890214
2023 SEMA3C stimulation of ER+ breast cancer cells activates MAPK and AKT signaling in a dose-dependent manner. SEMA3C silencing inhibits ER expression, MAPK and AKT signaling, and induces apoptosis. The SEMA3C pathway inhibitor B1SP Fc fusion protein attenuates SEMA3C-induced signaling via PlexinB1. Recombinant SEMA3C stimulation assay, siRNA knockdown, flow cytometry (apoptosis), Western blot for pathway activation, B1SP Fc fusion protein inhibition Cells Medium 37443749
2025 KLF6 recruits the PCAF-p300/CBP complex to the SEMA3C locus, increasing H3K23 succinylation and cooperating with FOSL2 to transcriptionally upregulate SEMA3C; SEMA3C in turn modulates the Wnt/β-catenin pathway (upregulating MYC and FOSL2) in 5-FU-resistant colon cancer cells. CUT&Tag, ATAC-seq, RNA-seq, ChIP assays for KLF6 and FOSL2 binding, knockdown of KLF6 and FOSL2 Experimental & Molecular Medicine Medium 40082673

Source papers

Stage 0 corpus · 36 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2014 Sema3C promotes the survival and tumorigenicity of glioma stem cells through Rac1 activation. Cell reports 99 25464848
2015 Bcl11a (Ctip1) Controls Migration of Cortical Projection Neurons through Regulation of Sema3c. Neuron 88 26182416
2021 MAOA promotes prostate cancer cell perineural invasion through SEMA3C/PlexinA2/NRP1-cMET signaling. Oncogene 76 33420365
2018 SEMA3C drives cancer growth by transactivating multiple receptor tyrosine kinases via Plexin B1. EMBO molecular medicine 68 29348142
2015 Neural crest-derived SEMA3C activates endothelial NRP1 for cardiac outflow tract septation. The Journal of clinical investigation 59 26053665
2017 Regulation of Sema3c and the Interaction between Cardiac Neural Crest and Second Heart Field during Outflow Tract Development. Scientific reports 46 28754980
2024 Semaphorin 3C (Sema3C) reshapes stromal microenvironment to promote hepatocellular carcinoma progression. Signal transduction and targeted therapy 40 38956074
2021 FOXM1 accelerates wound healing in diabetic foot ulcer by inducing M2 macrophage polarization through a mechanism involving SEMA3C/NRP2/Hedgehog signaling. Diabetes research and clinical practice 37 34742786
2019 Opposing Effects of Neuropilin-1 and -2 on Sensory Nerve Regeneration in Wounded Corneas: Role of Sema3C in Ameliorating Diabetic Neurotrophic Keratopathy. Diabetes 32 30679185
2018 Developmental Upregulation of Ephrin-B1 Silences Sema3C/Neuropilin-1 Signaling during Post-crossing Navigation of Corpus Callosum Axons. Current biology : CB 31 29779877
2021 LETR1 is a lymphatic endothelial-specific lncRNA governing cell proliferation and migration through KLF4 and SEMA3C. Nature communications 27 33568674
2012 Motoneuronal Sema3C is essential for setting stereotyped motor tract positioning in limb-derived chemotropic semaphorins. Development (Cambridge, England) 27 22899844
2023 Sema3C signaling is an alternative activator of the canonical WNT pathway in glioblastoma. Nature communications 25 37080989
2022 SEMA3C Supports Pancreatic Cancer Progression by Regulating the Autophagy Process and Tumor Immune Microenvironment. Frontiers in oncology 23 35785187
2015 High level of Sema3C is associated with glioma malignancy. Diagnostic pathology 22 26032848
2019 The Anti-Tumorigenic Activity of Sema3C in the Chick Embryo Chorioallantoic Membrane Model. International journal of molecular sciences 16 31726800
2007 Selenium modification of nucleic acids: preparation of oligonucleotides with incorporated 2'-SeMe-uridine for crystallographic phasing of nucleic acid structures. Nature protocols 16 17406626
2018 Importance of the putative furin recognition site 742RNRR745 for antiangiogenic Sema3C activity in vitro. Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas 11 30304095
2025 KLF6-mediated recruitment of the p300 complex enhances H3K23su and cooperatively upregulates SEMA3C with FOSL2 to drive 5-FU resistance in colon cancer cells. Experimental & molecular medicine 10 40082673
2016 A Sema3C Mutant Resistant to Cleavage by Furin (FR-Sema3C) Inhibits Choroidal Neovascularization. PloS one 9 28036336
2025 Cancer-associated fibroblast-derived SEMA3C facilitates colorectal cancer liver metastasis via NRP2-mediated MAPK activation. Proceedings of the National Academy of Sciences of the United States of America 8 40402249
2019 Effects of Notch signalling on the expression of SEMA3C, HMGA2, CXCL14, CXCR7, and CCL20 in breast cancer. Turkish journal of biology = Turk biyoloji dergisi 7 30930637
2023 Dependency of Tamoxifen Sensitive and Resistant ER+ Breast Cancer Cells on Semaphorin 3C (SEMA3C) for Growth. Cells 6 37443749
2021 Whole-genome sequencing identifies functional noncoding variation in SEMA3C that cosegregates with dyslexia in a multigenerational family. Human genetics 6 34076780
2020 Spatial association of SEMA3C with nerve endings/terminal Schwann cells in hair follicle isthmus region. International journal of developmental neuroscience : the official journal of the International Society for Developmental Neuroscience 5 32954569
2024 Clinically-observed FOXA1 mutations upregulate SEMA3C through transcriptional derepression in prostate cancer. Scientific reports 4 38528115
2012 The karyomastigont as an evolutionary seme. The Quarterly review of biology 4 23397796
2021 SEMA3C induces androgen synthesis in prostatic stromal cells through paracrine signaling. The Prostate 3 33503318
2024 SEMA3C promotes thyroid cancer via the Wnt/β-catenin pathway. Experimental cell research 2 39667698
2026 Tumor-stroma contributes to immunotherapeutic resistance in non-small cell lung cancer via SEMA3C-mediated immunosuppressive tumor microenvironment. Translational oncology 1 41558146
2025 The novel protein SEMA3C-319aa triggers glutathione metabolism-dependent ferroptosis in gastric cancer. Oncogene 1 40954198
2026 Silencing MALAT1 represses pathological progression, inflammation, and vascular smooth muscle cell phenotype switching by regulating the SEMA3C-mediated Smad pathway in intracranial aneurysms. Frontiers in cellular neuroscience 0 41890214
2026 A LINE-1 retrotransposon promotes SEMA3C expression as a cis-regulatory enhancer to sustain breast cancer stem cell survival. Science China. Life sciences 0 41984404
2025 SEMA3C regulates tumor-associated macrophage phenotype and influences lung cancer cell migration and invasion through VNN1. Human & experimental toxicology 0 40901786
2025 Astrocyte SEMA3C reduction improves Rett Syndrome phenotypes. bioRxiv : the preprint server for biology 0 41279175
2024 A Pilot Study of the Role of Semaphorin 4A (sema4A) and 3C (sema3C) in Non-Muscle-Invasive Bladder Cancer (NMIBC). Biomedicines 0 39457718