Affinage

S100A14

Protein S100-A14 · UniProt Q9HCY8

Length
104 aa
Mass
11.7 kDa
Annotated
2026-04-28
63 papers in source corpus 27 papers cited in narrative 27 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

S100A14 is an EF-hand-containing S100 family member that functions as a context-dependent signaling scaffold linking calcium-independent protein-protein interactions to transcriptional and post-translational control of cell proliferation, differentiation, invasion, and immune modulation. Structurally, S100A14 homodimerizes but does not bind calcium, adopting a semi-open apo conformation due to loss of canonical EF-hand ligands (PMID:23197251). Extracellularly, S100A14 signals through RAGE to activate ERK1/2 and NF-κB, driving chemokine secretion (CCL2, CXCL5) that promotes metastasis, and engages TLR4 on monocytes and astrocytes to stimulate innate immune activation and immunosuppressive niche formation (PMID:21559403, PMID:32483412, PMID:30422902, PMID:41691987). Intracellularly, S100A14 directly binds HER2 to potentiate PI3K/AKT and MAPK signaling (PMID:24285542), heterodimerizes with S100A16 to destabilize p53 and suppress p21 (PMID:24086685, PMID:41799516), promotes proteasomal degradation of IRAK1 and STAT3 to inhibit NF-κB and PD-L1 expression (PMID:32555330, PMID:35858011), and stabilizes glutaminase by blocking its phosphorylation-dependent ubiquitination to reduce oxidative stress (PMID:40217256).

Mechanistic history

Synthesis pass · year-by-year structured walk · 13 steps
  1. 2002 Medium

    Identification of S100A14 as a new S100 family member with cytoplasmic and plasma membrane localization established its basic molecular identity and subcellular context.

    Evidence cDNA cloning with epitope-tag immunofluorescence and subcellular fractionation in lung carcinoma and COS cells

    PMID:11944983

    Open questions at the time
    • No endogenous antibody validation at this stage
    • Functional role entirely unknown
    • Metal-binding properties not tested
  2. 2009 High

    Discovery of a functional p53-binding site in the S100A14 promoter placed S100A14 as a direct p53 transcriptional target, establishing the first regulatory link to a major tumor suppressor.

    Evidence Promoter mutagenesis, reporter assays, and SNP (461G>A) expression analysis in vitro and in vivo

    PMID:19351828

    Open questions at the time
    • Whether p53 activation or repression of S100A14 is context-dependent was not resolved
    • Downstream effectors of S100A14 were unknown
  3. 2010 High

    Bidirectional manipulation of S100A14 in oral cancer cells revealed it suppresses invasion by downregulating MMP1/MMP9, providing the first direct evidence for a functional role in invasion regulation.

    Evidence Retroviral overexpression, siRNA knockdown, Matrigel invasion assay, zymography

    PMID:21074410

    Open questions at the time
    • Mechanism connecting S100A14 to MMP transcription was not established
    • Generalizability to other cancer types unclear
  4. 2011 High

    Demonstration that extracellular S100A14 binds RAGE and activates ERK1/2 and NF-κB revealed a receptor-mediated extracellular signaling function, with EF-hand mutagenesis confirming structural requirements for activity; concurrently, intracellular S100A14 was shown to activate the p53/p21 axis and induce G1 arrest.

    Evidence Co-IP, dominant-negative RAGE, RAGE antagonist peptide, EF-hand mutants, caspase assays (PMID:21559403); retroviral overexpression with p53 shRNA epistasis (PMID:22032898)

    PMID:21559403 PMID:22032898

    Open questions at the time
    • Whether RAGE and p53 pathways converge or represent independent S100A14 functions was unresolved
    • Dose-dependent switch between proliferation and apoptosis mechanism unclear
  5. 2012 High

    NMR structure of apo S100A14 revealed it does not bind Ca²⁺ and adopts a semi-open conformation, fundamentally distinguishing it from canonical S100 proteins and resolving the paradox of its classification as a calcium-binding protein.

    Evidence NMR solution structure determination with metal-binding assays

    PMID:23197251

    Open questions at the time
    • How S100A14 achieves ligand recognition without calcium-induced conformational change was not explained
    • No structure of S100A14 in complex with any partner
  6. 2012 High

    Mechanistic epistasis experiments connected S100A14 to p53 transactivity and stability, with p53-dependent transrepression of MMP-2 explaining S100A14's pro-invasive phenotype in esophageal cancer.

    Evidence Reporter assays, Co-IP for p53, MMP-2 inhibitor rescue in esophageal and breast cancer cells

    PMID:22451655

    Open questions at the time
    • Whether S100A14 directly binds p53 or acts through an intermediary was not definitively resolved
    • Context dependency (pro-invasive in esophageal vs. anti-invasive in oral cancer) unexplained
  7. 2013 High

    Identification of S100A16 as the sole direct binding partner of S100A14 by yeast two-hybrid, with unidirectional post-translational stabilization, established a functional heterodimerization axis; simultaneously, direct binding to HER2 and JunB-driven transcription were established.

    Evidence Yeast two-hybrid, reciprocal Co-IP, cycloheximide chase (PMID:24086685); Co-IP, GST pull-down, mutant mapping for HER2 (PMID:24285542); ChIP and reporter assay for JunB (PMID:24107296)

    PMID:24086685 PMID:24107296 PMID:24285542

    Open questions at the time
    • How the S100A14-S100A16 heterodimer differs structurally from the S100A14 homodimer was unknown
    • Whether HER2 and S100A16 binding are mutually exclusive was untested
    • Functional consequences of S100A14-S100A16 interaction beyond protein stability were unclear
  8. 2014 High

    KLF4 was identified as a direct transcriptional activator of S100A14 through GC-rich promoter elements, adding to the growing network of transcription factors (p53, JunB, KLF4) controlling S100A14 expression.

    Evidence ChIP, promoter deletion/mutation reporter assays, stable shRNA knockdown with migration readout

    PMID:24532790

    Open questions at the time
    • Integration of multiple transcription factor inputs at the S100A14 promoter was not modeled
    • Chromatin context of KLF4 binding not explored
  9. 2016 Medium

    SOX2 was found to bind the 3'-UTR of S100A14 mRNA as an RNA-binding protein, stabilizing the transcript post-transcriptionally — an unusual mechanism for a transcription factor.

    Evidence CLIP, RNase H mapping, EGFP-3'UTR reporter assay, siRNA epistasis in urothelial carcinoma

    PMID:28955911

    Open questions at the time
    • SOX2 RNA-binding specificity determinants and generalizability to other mRNAs not established
    • Single lab finding
    • Structural basis of SOX2-S100A14 mRNA interaction unknown
  10. 2020 High

    Two studies resolved opposing S100A14 roles in NF-κB signaling: extracellular S100A14 activates RAGE-NF-κB to drive CCL2/CXCL5-dependent breast cancer metastasis, while intracellular S100A14 suppresses NF-κB in nasopharyngeal cancer by promoting IRAK1 proteasomal degradation.

    Evidence RNA-Seq, secreted proteomics, NF-κB ChIP, S100A14 KO, mouse metastasis (PMID:32483412); ubiquitination assays, bidirectional genetic manipulation, in vivo motility (PMID:32555330)

    PMID:32483412 PMID:32555330

    Open questions at the time
    • How context (intracellular vs. extracellular, cell type) determines opposing NF-κB outcomes is not mechanistically resolved
    • E3 ligase recruited by S100A14 for IRAK1 ubiquitination not identified
  11. 2022 High

    S100A14 was shown to directly interact with STAT3 and promote its proteasomal degradation, suppressing PD-L1 expression in colorectal cancer; separately, TP63/SOX2/EP300 were found to co-occupy an S100A14 enhancer whose disruption promotes esophageal tumorigenesis.

    Evidence Co-IP of S100A14-STAT3, proteasome inhibitor rescue (PMID:35858011); ChIP for TP63/SOX2/EP300, enhancer CRISPR disruption, 4NQO mouse model (PMID:35917972)

    PMID:35858011 PMID:35917972

    Open questions at the time
    • E3 ligase mediating STAT3 degradation not identified
    • Whether enhancer disruption effects are solely S100A14-dependent or involve neighboring genes not fully excluded
  12. 2025 High

    S100A14 was found to bind glutaminase (GLS), blocking phosphorylation at Y308/S314 and subsequent ubiquitination, thereby stabilizing GLS and reducing oxidative stress in hepatocellular carcinoma; additionally, Mfsd2a was identified as a physical partner that enhances S100A14 expression to inhibit STAT3.

    Evidence Co-IP with MS identification, phosphosite mapping, ubiquitination assay, xenograft (PMID:40217256); Co-IP/MS and STAT3 activator rescue (PMID:39806334)

    PMID:39806334 PMID:40217256

    Open questions at the time
    • Kinase phosphorylating GLS at Y308/S314 not identified
    • Mechanism by which Mfsd2a enhances S100A14 expression unknown
    • Whether GLS stabilization occurs in non-cancer contexts untested
  13. 2026 Medium

    Extracellular vesicle-delivered S100A14 was shown to reprogram brain astrocytes by targeting PIAS3 (activating STAT3) and TLR4 (activating NF-κB), establishing S100A14 as a key mediator of immunosuppressive brain pre-metastatic niche formation; the S100A14-S100A16 axis was further shown to destabilize p53 in pancreatic cancer.

    Evidence DIA proteomics, intracardiac mouse model, Co-IP for PIAS3, CETSA/DARTS (PMID:41961478); TMT proteomics, TLR4-dependent astrocyte co-culture (PMID:41691987); Co-IP, CHX chase, p53 reporter assay (PMID:41799516)

    PMID:41691987 PMID:41799516 PMID:41961478

    Open questions at the time
    • All three findings from single labs; independent replication needed
    • How S100A14 is selectively loaded into EVs is unknown
    • Whether PIAS3 and TLR4 engagement by S100A14 occurs simultaneously or in distinct EV subpopulations is unresolved
    • Structural basis of S100A14-PIAS3 interaction not determined

Open questions

Synthesis pass · forward-looking unresolved questions
  • Key unresolved questions include: the structural basis of S100A14's calcium-independent partner recognition; identification of E3 ligases it recruits for IRAK1 and STAT3 degradation; the mechanism determining whether S100A14 activates or suppresses NF-κB/STAT3 in different cell types; and whether its EV-mediated extracellular functions are relevant in normal physiology.
  • No co-crystal or cryo-EM structure of S100A14 with any partner
  • No unifying model for context-dependent pro- vs. anti-metastatic activity
  • Normal physiological role outside cancer poorly studied

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0098772 molecular function regulator activity 5 GO:0060090 molecular adaptor activity 3
Localization
GO:0005576 extracellular region 5 GO:0031410 cytoplasmic vesicle 2 GO:0005829 cytosol 1 GO:0005886 plasma membrane 1
Pathway
R-HSA-162582 Signal Transduction 5 R-HSA-168256 Immune System 3 R-HSA-392499 Metabolism of proteins 3 R-HSA-74160 Gene expression (Transcription) 3 R-HSA-5357801 Programmed Cell Death 2
Partners
AGERERBB2GLSIRAK1PIAS3S100A16STAT3TP53
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 was identified as a new S100 family member with two EF-hand Ca2+-binding domains; epitope-tagged S100A14 localizes to the cytoplasm with association to the plasma membrane and perinuclear area in lung carcinoma and monkey cell lines. cDNA cloning, sequence analysis, epitope-tag transfection with immunofluorescence/subcellular fractionation Genomics Medium 11944983
2011 Extracellular S100A14 binds to RAGE (receptor for advanced glycation end products) in esophageal squamous cell carcinoma cells, activating ERK1/2 MAPK and NF-κB signaling to stimulate cell proliferation at low doses; mutation of the N-EF hand (E39A, E45A) reduces S100A14-induced cell proliferation and ERK1/2 activation. At high doses, S100A14 induces apoptosis via the mitochondrial pathway (caspase-3, -9, PARP), partially RAGE-dependent. Co-immunoprecipitation, siRNA knockdown of RAGE, dominant-negative RAGE construct, RAGE antagonist peptide, EF-hand point mutagenesis, ERK1/2 and NF-κB activity assays, caspase activation assays PloS one High 21559403
2012 S100A14 promotes cell motility and invasiveness of esophageal squamous cell carcinoma cells by upregulating MMP-2 expression through a p53-dependent mechanism: S100A14 affects p53 transactivity and stability, and p53 transrepresses MMP-2 transcription; MMP-2 inhibition partially reverses the invasive phenotype. Ectopic overexpression, MMP-2 inhibitor treatment, series of biochemical assays (reporter assays, Co-IP for p53 interaction), RT-qPCR in human breast cancer specimens The Journal of biological chemistry High 22451655
2012 The solution structure of homodimeric human S100A14 in the apo state was solved by NMR, showing that S100A14 does not bind calcium ions and adopts a 'semi-open' conformation; lack of two canonical EF-hand ligands explains negligible Ca2+ affinity; exposed cysteines and histidine cause precipitation in the presence of zinc(II) or copper(II). NMR solution structure determination, metal-binding assays Journal of biological inorganic chemistry High 23197251
2013 S100A14 directly binds to HER2 via co-immunoprecipitation and pull-down assays; the binding requires residues 956–1154 of the HER2 intracellular domain and residue 83 of S100A14; S100A14 silencing decreases HER2 phosphorylation and downstream PI3K/AKT and MAPK/ERK signaling and reduces HER2-stimulated cell proliferation. Co-immunoprecipitation, GST pull-down, deletion/point mutant mapping, siRNA knockdown, phosphorylation assays, proliferation assays The Journal of biological chemistry High 24285542
2013 S100A14 interacts with S100A16 as its single binding partner identified by yeast two-hybrid screen, confirmed by co-immunoprecipitation and co-immunofluorescence; overexpression of S100A14 leads to concomitant upregulation of S100A16 protein (but not mRNA), suggesting post-transcriptional regulation; the regulation is unidirectional (S100A16 overexpression does not affect S100A14). Yeast two-hybrid screen, co-immunoprecipitation, double indirect immunofluorescence, retroviral overexpression and knockdown, cycloheximide chase, qRT-PCR PloS one High 24086685
2013 S100A14 is transcriptionally regulated by JunB, which binds the S100A14 promoter and controls expression during esophageal cancer cell differentiation; S100A14 mediates calcium-induced G1-phase cell cycle arrest and promotes expression of late differentiation markers involucrin (IVL) and filaggrin (FLG). ChIP, promoter reporter assays, overexpression and siRNA knockdown, cell cycle analysis, qRT-PCR for differentiation markers Molecular cancer research High 24107296
2009 The S100A14 gene contains a functional p53-binding site in its promoter; a SNP (461G>A) disrupts this p53-binding site and is associated with decreased S100A14 expression in vitro and in vivo, placing S100A14 downstream of p53 transcriptional regulation. DNA sequencing, p53-binding site mutagenesis, reporter assays, in vitro and in vivo expression analysis, case-control study Cancer research High 19351828
2011 Overexpression of S100A14 in oral squamous carcinoma cells (harboring wild-type p53) induces G1-arrest with upregulation of p21; nuclear accumulation of p53 occurs upon S100A14 overexpression; shRNA-mediated p53 silencing partially suppresses S100A14-induced p21 upregulation, indicating functional linkage between S100A14 and the p53/p21 axis. Retroviral overexpression, shRNA knockdown of p53, cell cycle analysis, Western blot for p21 and nuclear p53 Oral oncology Medium 22032898
2010 S100A14 regulates invasion of oral squamous cell carcinoma cells by modulating MMP1 and MMP9 expression: retroviral overexpression of S100A14 decreases invasive potential and downregulates MMP1 and MMP9 mRNA and MMP9 gelatinolytic activity, while siRNA knockdown increases invasion. Retroviral overexpression, siRNA knockdown, Matrigel invasion assay, PCR array, qRT-PCR, zymography European journal of cancer High 21074410
2014 KLF4 transcription factor directly binds two conserved GC-rich DNA segments within the S100A14 promoter, driving S100A14 transcriptional activation in response to TPA; stable silencing of KLF4 suppresses TPA-induced S100A14 upregulation and breast cancer cell migration. ChIP, promoter deletion/mutation analysis, reporter assays, stable shRNA knockdown, migration assay The Journal of biological chemistry High 24532790
2017 S100A14 induces differentiation of gastric cancer cells by upregulating E-cadherin and PGII expression, and inhibits metastasis by blocking store-operated Ca2+ influx through suppression of Orai1 and STIM1 expression, leading to FAK activation, focal adhesion assembly, and MMP downregulation. Overexpression and knockdown, Western blot for E-cadherin/PGII/Orai1/STIM1/FAK/MMPs, Ca2+ influx assay, migration/invasion assays, in vivo mouse model Cell death & disease Medium 28726786
2020 S100A14 promotes breast cancer metastasis by upregulating expression and secretion of CCL2 and CXCL5 via RAGE-NF-κB-mediated transcription; NF-κB ChIP confirmed binding to CCL2/CXCL5 promoters; S100A14 knockout abolishes this effect. RNA-Seq, secreted proteomics, ChIP for NF-κB, ELISA, transwell assay, neutralizing antibodies, S100A14 knockout and overexpression, mouse metastasis experiments 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 loop that can be disrupted by the IRAK1 inhibitor T2457. Gain- and loss-of-function studies, ubiquitination assays, Western blot for IRAK1 and NF-κB pathway, in vitro and in vivo motility assays, IHC of 202 NPC samples Oncogene High 32555330
2022 S100A14 inhibits PD-L1 expression in colorectal cancer by directly interacting with STAT3 and inducing its proteasome-mediated degradation; gain-of-S100A14 reduces STAT3-driven PD-L1 transcription, while loss-of-S100A14 increases PD-L1, cancer stem cell phenotypes, and chemoresistance. Co-IP of S100A14-STAT3, proteasome inhibitor rescue, PD-L1 expression assays, gain/loss-of-function in vitro and in vivo, chemoresistant CRC subline models Clinical and translational medicine High 35858011
2016 SOX2 binds the 3'-UTR of S100A14 mRNA via a stem-loop structure, stabilizing S100A14 mRNA and enhancing its expression; depletion of SOX2 decreases S100A14 mRNA and protein levels, and knockdown of S100A14 phenocopies SOX2 depletion in increasing cell mobility in urothelial carcinoma. Oligomer-directed RNase H digestion, CLIP (cross-linking immunoprecipitation), EGFP-3'UTR reporter assay, mobility shift assay, siRNA knockdown, cell growth and migration assays Biochemistry and biophysics reports Medium 28955911
2015 S100A14 overexpression in cervical cancer cells promotes EMT by increasing N-cadherin and Vimentin while decreasing E-cadherin; S100A14 overexpression increases G2/M phase proportion, proliferation, migration, and invasion, while knockdown reverses these effects. Lentiviral overexpression and knockdown, cell cycle analysis, transwell migration and invasion assays, Western blot for EMT markers American journal of cancer research Medium 26101712
2019 Extracellular S100A14 protein activates NK cells in a PBMC co-culture system (but not purified NK cells alone); treatment of purified monocytes with recombinant S100A14 induces TNF-alpha secretion and promotes NK cell CD69 activation via a TLR4-dependent interaction in co-culture. Recombinant protein treatment, PBMC/purified NK/monocyte co-culture, TLR4 blocking, ELISA for TNF-alpha, flow cytometry for CD69 Journal of acquired immune deficiency syndromes Medium 30422902
2022 ZHX2 transcriptionally inhibits S100A14 by binding to the S100A14 promoter; ZHX2 knockdown promotes thyroid cancer cell migration, an effect attenuated by S100A14 inhibition, placing S100A14 downstream of ZHX2 in this pro-metastatic axis. ChIP for ZHX2 at S100A14 promoter, ZHX2 and S100A14 knockdown, migration assay, wound healing, in vivo lung metastasis model Cancer cell international Medium 35151335
2022 TP63 transcriptionally activates S100A14 expression by occupying its enhancer region together with SOX2 and EP300; disruption of this enhancer reduces S100A14 expression and dramatically promotes 4NQO-induced ESCC tumorigenesis in mice. ChIP for TP63/SOX2/EP300 at S100A14 enhancer, enhancer disruption (CRISPR or deletion), 4NQO mouse tumorigenesis model, survival analysis Cancer letters High 35917972
2024 CTBP1-AS lncRNA blocks TP63-mediated transcriptional activation of S100A14, thereby reducing S100A14 expression; CTBP1-AS silencing suppresses proliferation, migration, invasion and tumorigenicity of prostate cancer cells, while TP63 overexpression further weakens malignant phenotype unless S100A14 is artificially silenced. Bioinformatics, qRT-PCR, Western blot, lentiviral overexpression/silencing, transcriptional activation assays, proliferation/apoptosis/migration/invasion assays, epistasis rescue experiment Cancer science Medium 38476086
2025 S100A14 binds to glutaminase (GLS) and blocks its phosphorylation at Y308 and S314, which inhibits GLS ubiquitination and subsequent proteasomal degradation, thereby stabilizing GLS; this reduces oxidative stress in HCC cells and antagonizes sorafenib-induced apoptosis. Co-immunoprecipitation, mass spectrometry to identify GLS as S100A14 binding partner, phosphorylation site mapping, ubiquitination assays, cell viability assays, in vivo xenograft experiments Journal of translational medicine High 40217256
2025 Mfsd2a interacts with S100A14 (identified by Co-IP and mass spectrometry), enhancing S100A14 expression and thereby inhibiting STAT3 phosphorylation; this suppresses CRC cell proliferation, migration, invasion, EMT, and liver metastasis. Co-immunoprecipitation, mass spectrometry, immunofluorescence, Western blot for p-STAT3, in vitro functional assays, in vivo tumor growth and liver metastasis models, STAT3 activator rescue Journal of translational medicine Medium 39806334
2026 S100A14 in tumor-derived extracellular vesicles (EVs) directly targets PIAS3 in astrocytes to activate STAT3 signaling, reprogramming astrocytes to secrete pro-inflammatory chemokines (CCL2/CCL5/CXCL5) that recruit immunosuppressive MDSCs and promote brain metastasis; the natural compound germacrone disrupts the S100A14-PIAS3 interaction to suppress this pathway. DIA-based proteomics of EVs, intracardiac injection mouse model, non-contact co-culture, multiplex cytokine profiling, MDSCs recruitment transwell assay, Co-IP for S100A14-PIAS3 interaction, Western blot for STAT3, CETSA/DARTS for germacrone binding Advanced science Medium 41961478
2026 Extracellular S100A14 from tumor-derived EVs targets astrocytic TLR4, activating NF-κB signaling and reprogramming astrocytes to secrete IL-6, CCL2, and CXCL1, thereby recruiting polymorphonuclear and monocytic MDSCs and establishing an immunosuppressive brain niche promoting metastasis. TMT-based quantitative proteomics, intracardiac mouse model, non-contact co-culture with primary astrocytes, multiplex cytokine profiling, MDSCs transwell recruitment assay, CETSA/DARTS for curdione binding to S100A14 Phytomedicine Medium 41691987
2026 S100A14 directly interacts with S100A16 (confirmed by Co-IP); S100A14 stabilizes S100A16 protein through post-translational modification without transcriptional regulation; the S100A14/S100A16 axis reduces p53 protein stability and inhibits p53 transcriptional activity and downstream p21 expression in pancreatic cancer. Co-immunoprecipitation, CHX chase assay, dual-luciferase reporter assay for p53 transcriptional activity, Western blot, qRT-PCR, CCK-8, Transwell, apoptosis assays Oncology research Medium 41799516
2021 S100A14 promotes cell growth and inhibits EMT in prostate cancer through activating FAT1 expression and the downstream Hippo pathway; S100A14 suppresses proliferation and motility of prostate cancer cells, confirmed in vivo in mouse xenograft models. Overexpression and knockdown of S100A14, Western blot for FAT1 and Hippo pathway components, proliferation/apoptosis/migration/invasion assays, mouse xenograft experiments Human cell Medium 33890248

Source papers

Stage 0 corpus · 63 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2008 Chemotactic activity of S100A7 (Psoriasin) is mediated by the receptor for advanced glycation end products and potentiates inflammation with highly homologous but functionally distinct S100A15. Journal of immunology (Baltimore, Md. : 1950) 144 18606705
2012 Vitamin D analog calcipotriol suppresses the Th17 cytokine-induced proinflammatory S100 "alarmins" psoriasin (S100A7) and koebnerisin (S100A15) in psoriasis. The Journal of investigative dermatology 107 22402441
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
2010 Novel S100A7 (psoriasin)/S100A15 (koebnerisin) subfamily: highly homologous but distinct in regulation and function. Amino acids 68 20596736
2007 S100A15, an antimicrobial protein of the skin: regulation by E. coli through Toll-like receptor 4. The Journal of investigative dermatology 66 17625598
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
2015 Leukocyte-derived koebnerisin (S100A15) and psoriasin (S100A7) are systemic mediators of inflammation in psoriasis. Journal of dermatological science 55 26055798
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 50 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 49 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
2007 Human S100A15 splice variants are differentially expressed in inflammatory skin diseases and regulated through Th1 cytokines and calcium. Experimental dermatology 33 17620096
2013 S100A14: novel modulator of terminal differentiation in esophageal cancer. Molecular cancer research : MCR 29 24107296
2013 Opposing functions of psoriasin (S100A7) and koebnerisin (S100A15) in epithelial carcinogenesis. Current opinion in pharmacology 28 23664757
2014 The role of S100A14 in epithelial ovarian tumors. Oncotarget 27 24939856
2014 The antimicrobial peptides psoriasin (S100A7) and koebnerisin (S100A15) suppress extracellular matrix production and proliferation of human fibroblasts. Skin pharmacology and physiology 26 25502330
2016 KCNN4 and S100A14 act as predictors of recurrence in optimally debulked patients with serous ovarian cancer. Oncotarget 25 27270322
2021 S100A14 promotes progression and gemcitabine resistance in pancreatic cancer. Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.] 24 33579599
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 24 24532790
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 Structural characterization of S100A15 reveals a novel zinc coordination site among S100 proteins and altered surface chemistry with functional implications for receptor binding. BMC structural biology 19 22747601
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
2012 Solution structure and dynamics of human S100A14. Journal of biological inorganic chemistry : JBIC : a publication of the Society of Biological Inorganic Chemistry 18 23197251
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 14 32922043
2017 Increased S100A15 expression and decreased DNA methylation of its gene promoter are involved in high metastasis potential and poor outcome of lung adenocarcinoma. Oncotarget 14 28498804
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
2013 Expression and function of psoriasin (S100A7) and koebnerisin (S100A15) in the brain. Infection and immunity 9 23478321
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
2019 Identification of S100A14 as a metastasis-promoting molecule in a murine organotropic metastasis model. Clinical & experimental metastasis 4 31263990
2024 LncRNA CTBP1-AS inhibits TP63-mediated activation of S100A14 during prostate cancer progression. Cancer science 3 38476086
2016 [Expression and regulatory mechanism of S100A14 in breast cancer]. Zhonghua zhong liu za zhi [Chinese journal of oncology] 3 27087370
2006 Purification, crystallization and preliminary X-ray diffraction of human S100A15. Acta crystallographica. Section F, Structural biology and crystallization communications 3 16682778
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
2023 Induction of Antimicrobial Protein S100A15 Expression by Oral Microbial Pathogens Is Toll-like Receptors-Dependent Activation of c-Jun-N-Terminal Kinase (JNK), p38, and NF-κB Pathways. International journal of molecular sciences 2 36982421
2017 S100A14 rs11548103 G>A polymorphism is associated with a decreased risk of esophageal cancer in a Chinese population. Oncotarget 2 29156846
2025 Serum circulating S100A7 and S100A15 DNA copies are elevated in patients with psoriasis and atopic dermatitis. The Journal of dermatology 1 40167275
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