Affinage

S100A14

Protein S100-A14 · UniProt Q9HCY8

Length
104 aa
Mass
11.7 kDa
Annotated
2026-06-10
50 papers in source corpus 27 papers cited in narrative 27 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 6/6 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

S100A14 is an EF-hand family calcium-binding protein that paradoxically does not bind Ca2+: its apo NMR solution structure reveals a semi-open homodimer in which the loss of two coordinating ligands in the canonical EF-hand abolishes Ca2+ affinity (PMID:23197251). It functions both as a secreted signaling ligand and as an intracellular regulator of cancer cell behavior. Extracellularly, S100A14 binds directly to RAGE to activate ERK1/2 and NF-κB, driving proliferation at low doses and mitochondrial apoptosis at high doses (PMID:21559403); this RAGE–NF-κB axis transcriptionally induces secreted chemokines (CCL2, CXCL5) that promote metastasis (PMID:32483412), and tumor-derived extracellular S100A14 reprograms astrocytes through TLR4–NF-κB and PIAS3–STAT3 to recruit immunosuppressive MDSCs and establish a brain metastatic niche (PMID:41961478, PMID:41691987). Intracellularly, S100A14 binds HER2 to potentiate its phosphorylation and downstream PI3K/AKT and MAPK/ERK signaling (PMID:24285542), and acts as a context-dependent regulator of invasion: it modulates MMP expression through a p53-dependent transcriptional axis (PMID:22451655, PMID:21074410) and induces G1 arrest and terminal differentiation via nuclear p53/p21 accumulation (PMID:22032898, PMID:24107296). S100A14 also suppresses oncogenic signaling by directing ubiquitin-proteasome degradation of IRAK1 to inhibit NF-κB (PMID:32555330) and of STAT3 to limit PD-L1 expression and stemness (PMID:35858011). It binds and stabilizes glutaminase by blocking its phosphorylation and ubiquitination, conferring sorafenib resistance (PMID:40217256), and forms a post-translationally regulated heterodimer with S100A16 (PMID:24086685, PMID:41799516). S100A14 is itself a downstream transcriptional target, regulated by p53 (PMID:19351828), JunB (PMID:24107296), KLF4 (PMID:24532790), and a TP63/SOX2/EP300 enhancer complex (PMID:35917972).

Mechanistic history

Synthesis pass · year-by-year structured walk · 17 steps
  1. 2002 Medium

    Establishing that S100A14 is a cytoplasmic, membrane-associated EF-hand protein gave the first structural and localization framework for an uncharacterized S100 family member.

    Evidence Epitope-tagged protein immunofluorescence and molecular cloning in lung carcinoma cell lines

    PMID:11944983

    Open questions at the time
    • No functional consequence linked to localization
    • Ca2+-binding capacity not tested
  2. 2009 Medium

    Identification of a p53-binding site disrupted by a SNP placed S100A14 transcriptionally downstream of p53, anchoring it within tumor-suppressor circuitry.

    Evidence Functional reporter assays of a 461G>A variant, RT-PCR, and case-control genetics

    PMID:19351828

    Open questions at the time
    • Direct promoter occupancy by p53 not shown in this study
    • Genetics is association-level
  3. 2012 High

    The apo NMR structure resolved the paradox of an EF-hand protein that cannot bind Ca2+, explaining its non-canonical semi-open conformation.

    Evidence NMR solution structure determination and metal-binding assays

    PMID:23197251

    Open questions at the time
    • Functional role of the semi-open conformation not defined
    • Physiological metal/ligand interactions not mapped
  4. 2011 High

    Demonstrating direct S100A14–RAGE binding identified the extracellular receptor through which S100A14 controls a dose-dependent proliferation/apoptosis switch.

    Evidence Reciprocal Co-IP, EF-hand mutagenesis, multiple RAGE-inhibition approaches, ERK/caspase readouts

    PMID:21559403

    Open questions at the time
    • Threshold determining proliferation versus apoptosis not defined
    • Did not establish secreted source in vivo
  5. 2012 High

    Connecting S100A14 to MMP regulation through p53 defined a transcriptional axis controlling invasion, while context dictated direction.

    Evidence Overexpression, inhibitor rescue, transactivation reporters, Matrigel invasion (JBC); contrasted with OSCC loss/gain-of-function and zymography

    PMID:21074410 PMID:22451655

    Open questions at the time
    • Opposing pro- and anti-invasive effects across cell types not mechanistically reconciled
    • p53-dependence varies with p53 status
  6. 2011 Medium

    Linking S100A14 to G1 arrest, p21 induction, and terminal differentiation established its tumor-suppressive, differentiation-promoting role in wild-type p53 contexts.

    Evidence Retroviral overexpression, shRNA p53 silencing, flow cytometry, differentiation marker analysis (Oral Oncol; Mol Cancer Res)

    PMID:22032898 PMID:24107296

    Open questions at the time
    • How nuclear p53 accumulation is triggered is unresolved
    • p21 induction only partly p53-dependent
  7. 2013 High

    Mapping a direct S100A14–HER2 interaction identified an intracellular mechanism by which S100A14 amplifies receptor tyrosine kinase signaling.

    Evidence Reciprocal Co-IP, pull-down, domain-mapping mutagenesis, phosphorylation and proliferation assays

    PMID:24285542

    Open questions at the time
    • Whether binding directly alters HER2 kinase activity versus stability not separated
    • Ca2+-independence of the interaction not tested
  8. 2013 High

    Discovery of the S100A14–S100A16 heterodimer and its unidirectional post-translational regulation revealed cross-talk within the S100 family.

    Evidence Yeast two-hybrid, Co-IP, co-immunofluorescence, cycloheximide chase, proteasome/lysosome inhibitor treatment

    PMID:24086685

    Open questions at the time
    • Degradation pathway stabilizing S100A16 not identified (proteasome/lysosome-independent)
    • Functional output of the heterodimer not defined here
  9. 2014 High

    Identifying JunB and KLF4 as direct promoter-binding activators placed S100A14 downstream of stress- and TPA-responsive transcription, linking its expression to motility programs.

    Evidence ChIP, promoter reporter assays, KLF4 silencing epistasis, migration assays

    PMID:24532790

    Open questions at the time
    • Interplay between the multiple upstream transcription factors not integrated
    • Signals selecting activator usage unknown
  10. 2014 Medium

    Demonstrating PI3K/Akt-dependent pro-tumorigenic effects in ovarian cancer established a context where S100A14 acts as a metastasis promoter, contrasting with its suppressive roles elsewhere.

    Evidence Lentiviral overexpression/knockdown, xenograft, PI3K/Akt pharmacological inhibition

    PMID:24939856

    Open questions at the time
    • Pathway assignment by inhibitor without direct epistasis
    • Upstream link to PI3K/Akt not molecularly defined
  11. 2017 Medium

    Linking S100A14 to suppression of Orai1/STIM1 store-operated Ca2+ entry and FAK activation provided a mechanism for its anti-metastatic, pro-differentiation effect in gastric cancer.

    Evidence Overexpression/knockdown, Ca2+ imaging, FAK/focal adhesion analysis, in vivo metastasis model

    PMID:28726786

    Open questions at the time
    • How a non-Ca2+-binding protein regulates Ca2+ channels is unexplained
    • Single lab
  12. 2020 High

    Defining a RAGE–NF-κB chemokine output (CCL2/CXCL5) and a counterbalancing IRAK1-degradation mechanism clarified how S100A14 both activates and restrains NF-κB depending on context.

    Evidence RNA-Seq, secreted proteomics, ChIP, neutralizing antibody, metastasis models; separately ubiquitin-proteasome and NF-κB reporter assays for IRAK1

    PMID:32483412 PMID:32555330

    Open questions at the time
    • What determines pro- versus anti-NF-κB outcome across tumor types not resolved
    • E3 ligase for IRAK1 degradation not identified
  13. 2022 High

    Discovery that S100A14 directly binds STAT3 to drive its proteasomal degradation linked S100A14 to immune evasion via PD-L1 and to stemness/chemoresistance.

    Evidence Co-IP, proteasome inhibitor treatment, PD-L1 reporter, recombinant protein rescue, in vivo model

    PMID:35858011

    Open questions at the time
    • E3 ligase mediating STAT3 degradation not identified
    • Reconciliation with STAT3-activating roles in other contexts unaddressed
  14. 2022 Medium

    Identifying ZHX2 as a repressor and a TP63/SOX2/EP300 enhancer as an activator extended the transcriptional control map and confirmed tumor-suppressive function in vivo.

    Evidence ChIP, enhancer disruption, 4NQO carcinogenesis model, knockdown migration assays

    PMID:35151335 PMID:35917972

    Open questions at the time
    • Coordination among the many transcriptional regulators not integrated
    • Single labs
  15. 2025 High

    Showing that S100A14 binds glutaminase and blocks its phosphorylation/ubiquitination defined a metabolic stabilization mechanism conferring sorafenib resistance.

    Evidence Co-IP/mass spectrometry, phosphosite mapping, ubiquitination assay, xenograft

    PMID:40217256

    Open questions at the time
    • Kinase/E3 ligase normally targeting GLS not identified
    • Generality beyond hepatocellular carcinoma untested
  16. 2026 Medium

    Demonstrating that EV-delivered S100A14 reprograms astrocytes via TLR4-NF-κB and PIAS3-STAT3 to recruit MDSCs established a non-cell-autonomous role in building a brain metastatic immunosuppressive niche.

    Evidence Quantitative proteomics, intracardiac brain metastasis models, astrocyte co-culture, MDSC recruitment assays, DARTS-based compound binding

    PMID:41691987 PMID:41961478

    Open questions at the time
    • PIAS3 versus TLR4 mechanisms from the same group not reconciled
    • Direct PIAS3 binding inferred from DARTS rather than reconstitution
  17. 2026 Medium

    Refining the S100A14–S100A16 axis showed the heterodimer destabilizes p53 to inhibit p21, providing a molecular basis for context-dependent pro-tumorigenic activity.

    Evidence Co-IP, CHX chase, dual-luciferase p53 activity assay, gain/loss-of-function

    PMID:41799516

    Open questions at the time
    • Mechanism of p53 destabilization not defined
    • No in vivo validation

Open questions

Synthesis pass · forward-looking unresolved questions
  • How a single non-Ca2+-binding protein switches between tumor-suppressive (p53/p21, IRAK1/STAT3 degradation, differentiation) and pro-metastatic (RAGE/NF-κB chemokine, PI3K/Akt, GLS stabilization, astrocyte reprogramming) programs across tissues remains unresolved.
  • No unified model linking conformation to opposing activities
  • E3 ligases for IRAK1/STAT3/GLS degradation unidentified
  • In vivo source and regulation of secreted versus intracellular pools unclear

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0098772 molecular function regulator activity 3 GO:0140096 catalytic activity, acting on a protein 3 GO:0048018 receptor ligand activity 2 GO:0140110 transcription regulator activity 2
Localization
GO:0005576 extracellular region 2 GO:0005886 plasma membrane 2 GO:0005634 nucleus 1 GO:0005829 cytosol 1
Pathway
R-HSA-1643685 Disease 4 R-HSA-162582 Signal Transduction 3 R-HSA-168256 Immune System 3 R-HSA-392499 Metabolism of proteins 3 R-HSA-1640170 Cell Cycle 2
Partners
GLSHER2IRAK1PIAS3RAGES100A16STAT3TLR4
Complex memberships
S100A14/S100A16 heterodimer

Evidence

Reading pass · 27 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2002 S100A14 protein localizes predominantly to the cytoplasm with association with the plasma membrane and perinuclear area in human lung carcinoma cell lines, as determined by epitope-tagged protein imaging. The protein contains two EF-hand Ca2+-binding domains and is encoded by a gene on chromosome 1q21. Epitope-tagged protein immunofluorescence/localization in cell lines; molecular cloning and sequence analysis Genomics Medium 11944983
2011 Extracellular S100A14 binds directly to RAGE (receptor for advanced glycation end products), activating ERK1/2 MAPK and NF-κB signaling to promote cell proliferation at low doses and apoptosis via the mitochondrial pathway (caspase-3, caspase-9, PARP activation) at high doses. Mutation of the N-EF hand (E39A, E45A) reduced S100A14-induced proliferation and ERK1/2 activation. RAGE inhibition (siRNA, dominant-negative construct, or antagonist peptide) blocked S100A14-induced effects. Co-immunoprecipitation, siRNA knockdown, dominant-negative overexpression, EF-hand point mutagenesis, RAGE antagonist peptide, ERK1/2 phosphorylation assay, caspase activity assay PloS one High 21559403
2012 S100A14 promotes cell motility and invasion by increasing MMP-2 expression and activity in a p53-dependent manner: S100A14 affects p53 transactivity and stability, and p53 in turn transrepresses MMP-2 transcription. Functional p53 is required for S100A14 to modulate MMP2 levels. Ectopic overexpression, MMP2-specific inhibitor rescue, reporter/transactivation assays, RT-qPCR, Western blot, Matrigel invasion assay The Journal of biological chemistry High 22451655
2012 Solution structure of homodimeric human S100A14 in the apo state was solved by NMR at physiological temperature. The protein does not bind Ca2+ ions and adopts a 'semi-open' conformation. Absence of two Ca2+-coordinating ligands in the canonical EF-hand site explains negligible Ca2+ affinity. Exposed cysteines and histidine cause precipitation in the presence of Zn2+ or Cu2+ ions. NMR solution structure determination; metal-binding assays Journal of biological inorganic chemistry High 23197251
2010 S100A14 overexpression decreases invasive potential of oral squamous cell carcinoma cells and is associated with downregulation of MMP1 and MMP9 mRNA and suppression of MMP9 gelatinolytic activity; siRNA-mediated knockdown increases invasiveness. S100A14 protein undergoes membrane-to-cytoplasm translocation in invading tumor islands. Retroviral overexpression, siRNA knockdown, Matrigel invasion assay, PCR array, qRT-PCR, gelatin zymography, immunohistochemistry European journal of cancer High 21074410
2011 S100A14 overexpression induces G1-phase cell cycle arrest and inhibits proliferation in oral carcinoma cells harboring wild-type p53, correlating with upregulation of p21. Nuclear accumulation of p53 occurs upon S100A14 overexpression. shRNA-mediated p53 silencing partially suppresses S100A14-induced p21 upregulation, indicating that p21 induction is at least partly p53-dependent. Retroviral overexpression, shRNA knockdown, cell cycle analysis (flow cytometry), Western blot, immunofluorescence Oral oncology High 22032898
2013 S100A14 directly binds HER2 via co-immunoprecipitation and pull-down assays. The interaction requires residues 956–1154 of the HER2 intracellular domain and residue 83 of S100A14. S100A14 silencing reduces HER2 phosphorylation and downstream PI3K/AKT and MAPK/ERK signaling and decreases HER2-stimulated cell proliferation. Co-immunoprecipitation, pull-down assay, domain-mapping mutagenesis, siRNA knockdown, phosphorylation assays, proliferation assay The Journal of biological chemistry High 24285542
2013 S100A14 interacts with S100A16 (identified by yeast two-hybrid screen and confirmed by co-immunoprecipitation and co-immunofluorescence). S100A14 overexpression upregulates S100A16 protein without increasing S100A16 mRNA, indicating post-transcriptional regulation. Regulation is unidirectional: S100A16 overexpression does not upregulate S100A14. The degradation of both proteins is independent of classical proteasomal and lysosomal pathways. Yeast two-hybrid screen, co-immunoprecipitation, double indirect immunofluorescence, retroviral overexpression/knockdown, cycloheximide chase assay, proteasome/lysosome inhibitor treatment PloS one High 24086685
2013 S100A14 expression is transcriptionally regulated by JunB, which binds directly to the S100A14 promoter. S100A14 promotes terminal differentiation of esophageal cancer cells and calcium-induced G1 arrest, and modulates expression of late differentiation markers involucrin (IVL) and filaggrin (FLG). Overexpression/knockdown, ChIP (JunB binding to S100A14 promoter), immunohistochemistry, RT-PCR, Western blot, cell cycle analysis Molecular cancer research Medium 24107296
2014 KLF4 transcriptionally activates S100A14 expression by binding directly to two conserved GC-rich elements in the S100A14 promoter in response to TPA treatment. KLF4 silencing suppresses TPA-induced breast cancer cell migration, demonstrating that TPA promotes cell motility through the KLF4–S100A14 axis. ChIP (KLF4 binding to S100A14 promoter), promoter reporter assays, stable KLF4 silencing, cell migration assay, Western blot The Journal of biological chemistry High 24532790
2014 S100A14 overexpression in epithelial ovarian cancer cells promotes cell proliferation, tumorigenesis, migration, and invasion through the PI3K/Akt pathway; knockdown inhibits these properties and reduces xenograft tumor growth. Lentiviral overexpression/knockdown, proliferation assay, migration/invasion assay, xenograft mouse model, PI3K/Akt pathway inhibition Oncotarget Medium 24939856
2017 S100A14 induces differentiation of gastric cancer cells, upregulating E-cadherin and PGII. S100A14 blocks store-operated Ca2+ influx by suppressing Orai1 and STIM1 expression, leading to FAK expression activation, focal adhesion assembly, and MMP downregulation, thereby suppressing metastasis. Overexpression/knockdown, Western blot, Ca2+ imaging/store-operated Ca2+ entry assay, FAK/focal adhesion analysis, invasion assay, in vivo metastasis model Cell death & disease Medium 28726786
2016 SOX2 binds directly to the 3'-UTR of S100A14 mRNA (identified as a stem-loop structure) and stabilizes S100A14 mRNA, increasing its expression. SOX2 depletion reduces S100A14 mRNA and protein; loss of either SOX2 or S100A14 increases cell growth and mobility in urothelial carcinoma cells. CLIP (cross-linking and immunoprecipitation), oligomer-directed RNase H digestion, EGFP-3'UTR reporter, RNA mobility shift assay, siRNA knockdown, cell migration and growth assays Biochemistry and biophysics reports Medium 28955911
2019 Extracellular recombinant S100A14 activates NK cells indirectly by first activating monocytes through a TLR4-dependent interaction to secrete TNF-alpha, which then activates NK cells (increased CD69) in co-culture. S100A14 does not activate purified NK cells alone. Recombinant protein treatment, co-culture assay, TLR4 inhibition, ELISA (TNF-alpha), flow cytometry (NK CD69) Journal of acquired immune deficiency syndromes Medium 30422902
2020 S100A14 promotes breast cancer metastasis by upregulating the expression and secretion of chemokines CCL2 and CXCL5 via RAGE-NF-κB–mediated transcription, as demonstrated by RNA-Seq, secreted proteomics, ChIP (NF-κB binding to CCL2/CXCL5 promoters), and neutralizing antibody experiments. S100A14 knockout/overexpression, RNA-Seq, secreted proteomics, ChIP, ELISA, transwell assay, neutralizing antibody, mouse metastasis model Theranostics High 32483412
2020 S100A14 suppresses NPC metastasis by promoting ubiquitin-proteasome-mediated degradation of IRAK1, thereby inhibiting NF-κB signaling and reversing EMT. S100A14 and IRAK1 form a feedback regulatory loop that can be disrupted by the IRAK1 inhibitor T2457. Gain/loss-of-function experiments, ubiquitin-proteasome pathway assays, NF-κB reporter, EMT marker analysis, IRAK1 inhibitor treatment, in vivo motility assays Oncogene High 32555330
2022 S100A14 directly interacts with STAT3 and induces its proteasome-mediated degradation, thereby inhibiting PD-L1 expression in colorectal cancer cells and suppressing cancer stem-like cell phenotypes and chemoresistance. Co-immunoprecipitation (S100A14–STAT3 interaction), proteasome inhibitor treatment, Western blot, PD-L1 reporter, gain/loss-of-function, in vivo tumor model, recombinant S100A14 protein treatment Clinical and translational medicine High 35858011
2022 ZHX2 transcription factor binds to the S100A14 promoter to suppress its transcription, thereby inhibiting S100A14-mediated thyroid cancer metastasis. ZHX2 knockdown-induced enhanced metastasis was attenuated by S100A14 inhibition. ChIP (ZHX2 binding to S100A14 promoter), ZHX2/S100A14 knockdown, migration assay, wound healing assay, in vivo lung metastasis model Cancer cell international Medium 35151335
2022 Disruption of an enhancer element (occupied by TP63, SOX2, and EP300) decreases S100A14 expression in ESCC. S100A14 deficiency promotes 4NQO-induced esophageal tumorigenesis and triggers an aberrant differentiation program in vivo. ChIP (TP63, SOX2, EP300 occupancy at S100A14 enhancer), enhancer deletion/disruption, 4NQO mouse carcinogenesis model, survival analysis, Western blot Cancer letters Medium 35917972
2021 S100A14 promotes prostate cancer cell growth and EMT by upregulating FAT1, which activates the Hippo signaling pathway. S100A14 knockdown suppresses tumor growth in vivo through the FAT1-Hippo axis. Overexpression/knockdown, Western blot (Hippo pathway components), proliferation/apoptosis assays, EMT marker analysis, xenograft mouse model Human cell Medium 33890248
2025 S100A14 binds directly to glutaminase (GLS) and blocks GLS phosphorylation at residues Y308 and S314, thereby inhibiting its ubiquitination and degradation. This GLS stabilization reduces oxidative stress in hepatocellular carcinoma cells and antagonizes sorafenib-induced apoptosis, conferring primary sorafenib resistance. Co-immunoprecipitation and mass spectrometry (S100A14–GLS interaction), GLS phosphorylation site mapping, ubiquitination assay, cell viability assay, xenograft mouse model, S100A14/GLS knockdown Journal of translational medicine High 40217256
2025 Mfsd2a interacts with S100A14 (confirmed by Co-IP and mass spectrometry) and enhances S100A14 expression, leading to inhibition of STAT3 phosphorylation and suppression of colorectal cancer progression and liver metastasis. STAT3 activator colivelin partially reverses the inhibitory effects of Mfsd2a overexpression. Co-immunoprecipitation, mass spectrometry, immunofluorescence, Western blot (p-STAT3), colivelin rescue experiment, in vitro and in vivo tumor models Journal of translational medicine Medium 39806334
2026 S100A14 stabilizes S100A16 protein through post-translational modification (without transcriptional regulation); the S100A14/S100A16 complex then reduces p53 protein stability and inhibits p53 transcriptional activity and downstream p21 expression, promoting pancreatic cancer progression. Co-IP confirms the S100A14–S100A16 physical interaction. Co-immunoprecipitation (S100A14–S100A16), CHX chase assay (protein stability), dual-luciferase assay (p53 transcriptional activity), gain/loss-of-function, Western blot Oncology research Medium 41799516
2026 Tumor-derived S100A14 in extracellular vesicles (EVs) directly targets PIAS3 in astrocytes to activate STAT3 signaling and promote secretion of CCL2, CCL5, and CXCL5, recruiting immunosuppressive MDSCs and establishing a brain immunosuppressive niche that promotes brain metastasis. The natural compound germacrone disrupts the S100A14–PIAS3 interaction to reverse this pathway. DIA-based proteomics, intracardiac injection brain metastasis mouse model, EV isolation and overexpression, non-contact co-culture, STAT3 signaling assays, MDSC recruitment transwell assay, CELTS/DARTS assays (germacrone binding to S100A14) Advanced science Medium 41961478
2026 Tumor-derived extracellular S100A14 targets astrocytic TLR4 to activate NF-κB signaling, reprogramming astrocytes to secrete IL-6, CCL2, and CXCL1, which recruit both polymorphonuclear and monocytic MDSCs and establish a brain immunosuppressive niche promoting brain metastasis. Curdione directly binds S100A14 to reverse this cascade. TMT-based quantitative proteomics, intracardiac injection brain metastasis mouse model, non-contact co-culture with primary astrocytes, multiplex cytokine profiling, MDSC recruitment transwell assay, CELTS/DARTS assays (curdione–S100A14 binding), ELISA Phytomedicine Medium 41691987
2024 The lncRNA CTBP1-AS blocks TP63-mediated transcriptional activation of S100A14 without affecting TP63 expression itself, thereby reducing S100A14 levels and promoting prostate cancer progression. TP63 overexpression partially rescues the malignant phenotype induced by CTBP1-AS, and this rescue is reversed by S100A14 silencing. Overexpression/knockdown of CTBP1-AS and TP63, Western blot, RT-qPCR, cell proliferation/migration/invasion assays, epistasis rescue experiments Cancer science Medium 38476086
2009 A single nucleotide polymorphism (461G>A) in the S100A14 locus disrupts a p53-binding site in the S100A14 regulatory region, resulting in decreased S100A14 expression in vitro and in vivo, placing S100A14 as a transcriptional target of p53. DNA sequencing, functional reporter assays (p53-binding site), RT-PCR, in vivo expression analysis, case-control genetics Cancer research Medium 19351828

Source papers

Stage 0 corpus · 50 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2011 S100A14 stimulates cell proliferation and induces cell apoptosis at different concentrations via receptor for advanced glycation end products (RAGE). PloS one 83 21559403
2002 Molecular cloning and characterization of the human S100A14 gene encoding a novel member of the S100 family. Genomics 71 11944983
2012 Involvement of S100A14 protein in cell invasion by affecting expression and function of matrix metalloproteinase (MMP)-2 via p53-dependent transcriptional regulation. The Journal of biological chemistry 63 22451655
2010 S100A14 regulates the invasive potential of oral squamous cell carcinoma derived cell-lines in vitro by modulating expression of matrix metalloproteinases, MMP1 and MMP9. European journal of cancer (Oxford, England : 1990) 52 21074410
2020 A S100A14-CCL2/CXCL5 signaling axis drives breast cancer metastasis. Theranostics 51 32483412
2013 S100A14, a member of the EF-hand calcium-binding proteins, is overexpressed in breast cancer and acts as a modulator of HER2 signaling. The Journal of biological chemistry 50 24285542
2010 Expression status of S100A14 and S100A4 correlates with metastatic potential and clinical outcome in colorectal cancer after surgery. Oncology reports 49 19956863
2011 S100A14 inhibits proliferation of oral carcinoma derived cells through G1-arrest. Oral oncology 47 22032898
2017 Calcium-binding protein S100A14 induces differentiation and suppresses metastasis in gastric cancer. Cell death & disease 39 28726786
2015 S100A14, a mediator of epithelial-mesenchymal transition, regulates proliferation, migration and invasion of human cervical cancer cells. American journal of cancer research 38 26101712
2020 S100A14 suppresses metastasis of nasopharyngeal carcinoma by inhibition of NF-kB signaling through degradation of IRAK1. Oncogene 37 32555330
2009 Functional role of S100A14 genetic variants and their association with esophageal squamous cell carcinoma. Cancer research 36 19351828
2013 S100A14 promotes the growth and metastasis of hepatocellular carcinoma. Asian Pacific journal of cancer prevention : APJCP 35 23886191
2013 S100A14: novel modulator of terminal differentiation in esophageal cancer. Molecular cancer research : MCR 29 24107296
2014 The role of S100A14 in epithelial ovarian tumors. Oncotarget 27 24939856
2016 KCNN4 and S100A14 act as predictors of recurrence in optimally debulked patients with serous ovarian cancer. Oncotarget 25 27270322
2014 12-O-tetradecanoylphorbol-13-acetate promotes breast cancer cell motility by increasing S100A14 level in a Kruppel-like transcription factor 4 (KLF4)-dependent manner. The Journal of biological chemistry 25 24532790
2021 S100A14 promotes progression and gemcitabine resistance in pancreatic cancer. Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.] 24 33579599
2013 S100A14 interacts with S100A16 and regulates its expression in human cancer cells. PloS one 23 24086685
2020 Upregulated lncRNA CASC9 Contributes to Progression of Non-Small Cell Lung Cancer Through Inhibition of miR-335-3p and Activation S100A14 Expression. OncoTargets and therapy 22 32606808
2015 Overexpression of S100A14 in human serous ovarian carcinoma. Oncology letters 21 26893702
2021 S100A14 inhibits cell growth and epithelial-mesenchymal transition (EMT) in prostate cancer through FAT1-mediated Hippo signaling pathway. Human cell 20 33890248
2012 Solution structure and dynamics of human S100A14. Journal of biological inorganic chemistry : JBIC : a publication of the Society of Biological Inorganic Chemistry 19 23197251
2022 S100A14: A novel negative regulator of cancer stemness and immune evasion by inhibiting STAT3-mediated programmed death-ligand 1 expression in colorectal cancer. Clinical and translational medicine 18 35858011
2017 Clinicopathological Significance of S100A14 Expression in Lung Adenocarcinoma. Oncology research and treatment 18 28950283
2012 Loss of S100A14 expression is associated with the progression of adenocarcinomas of the small intestine. Pathobiology : journal of immunopathology, molecular and cellular biology 18 23038644
2022 ZHX2 inhibits thyroid cancer metastasis through transcriptional inhibition of S100A14. Cancer cell international 17 35151335
2020 Long Noncoding RNA HIF1A-AS2 Promotes Non-Small Cell Lung Cancer Progression by the miR-153-5p/S100A14 Axis. OncoTargets and therapy 15 32922043
2022 Construction of immune-related signature and identification of S100A14 determining immune-suppressive microenvironment in pancreatic cancer. BMC cancer 11 35953822
2022 Disruption of enhancer-driven S100A14 expression promotes esophageal carcinogenesis. Cancer letters 10 35917972
2022 Circ_0003221 Downregulation Restrains Cervical Cancer Cell Growth, Metastasis and Angiogenesis by Governing the miR-139-3p/S100A14 Pathway. Reproductive sciences (Thousand Oaks, Calif.) 8 35023052
2022 Significance of a calcium-binding protein S100A14 expression in colon cancer progression. Journal of gastrointestinal oncology 7 35284114
2025 Mfsd2a suppresses colorectal cancer progression and liver metastasis via the S100A14/STAT3 axis. Journal of translational medicine 6 39806334
2020 A Clinicopathological Analysis of S100A14 Expression in Colorectal Cancer. In vivo (Athens, Greece) 6 31882495
2019 S100A14 Is Increased in Activated NK Cells and Plasma of HIV-Exposed Seronegative People Who Inject Drugs and Promotes Monocyte-NK Crosstalk. Journal of acquired immune deficiency syndromes (1999) 5 30422902
2018 DNA methylation patterns of the S100A14, POU2F3 and SFN genes in equine sarcoid tissues. Research in veterinary science 5 30086514
2016 SOX2 suppresses the mobility of urothelial carcinoma by promoting the expression of S100A14. Biochemistry and biophysics reports 5 28955911
2024 LncRNA CTBP1-AS inhibits TP63-mediated activation of S100A14 during prostate cancer progression. Cancer science 4 38476086
2019 Identification of S100A14 as a metastasis-promoting molecule in a murine organotropic metastasis model. Clinical & experimental metastasis 4 31263990
2016 [Expression and regulatory mechanism of S100A14 in breast cancer]. Zhonghua zhong liu za zhi [Chinese journal of oncology] 3 27087370
2025 Endogenous protein S100A14 stabilizes glutaminase to render hepatocellular carcinoma resistant to sorafenib. Journal of translational medicine 2 40217256
2024 Correlation of S100A4 and S100A14 Expression With Clinico-Pathological Features and Tumor Location in Colorectal Cancer Patients. Cureus 2 39205741
2024 The emerging role of S100A4 and S100A14 proteins in colorectal cancer progression. Cellular and molecular biology (Noisy-le-Grand, France) 2 39707769
2017 S100A14 rs11548103 G>A polymorphism is associated with a decreased risk of esophageal cancer in a Chinese population. Oncotarget 2 29156846
2025 S100A14 as a Potential Biomarker of the Colorectal Serrated Neoplasia Pathway. International journal of molecular sciences 1 40806532
2024 Mediation of circ_0007142 on miR-128-3p/S100A14 pathway to stimulate the progression of cervical cancer. Naunyn-Schmiedeberg's archives of pharmacology 1 38951152
2026 Tumor-derived S100A14 targeted astrocytes via TLR4 to Recruit myeloid-derived suppressor cells promoting brain metastasis and Curdione reversal effect. Phytomedicine : international journal of phytotherapy and phytopharmacology 0 41691987
2026 S100A14 Facilitates Pancreatic Cancer Progression via S100A16-Mediated p53 Suppression. Oncology research 0 41799516
2026 S100A14 in Tumor-Derived EVs Targets PIAS3 to Reprogram Astrocytes and Induce Immunosuppressive Microenvironment Promoting Brain Metastasis and Germacrone Reversal Effect. Advanced science (Weinheim, Baden-Wurttemberg, Germany) 0 41961478
2026 Lactylation-Associated Immune Metabolic Reprogramming Identifies S100A2 and S100A14 as Candidate Diagnostic Biomarkers in Primary Open-Angle Glaucoma: An Integrated Bulk and Single-Cell Transcriptomic Analysis. Genes 0 42074521

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