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CMTM4

CKLF-like MARVEL transmembrane domain-containing protein 4 · UniProt Q8IZR5

Length
234 aa
Mass
25.8 kDa
Annotated
2026-06-09
31 papers in source corpus 19 papers cited in narrative 19 extracted findings
Cross-family judge vs UniProt: tie faithfulness: 5/5 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

CMTM4 is a tetra-transmembrane MARVEL-domain protein that acts as a post-translational regulator of membrane protein stability, glycosylation, and endocytic trafficking across immune, vascular, and oncogenic contexts (PMID:28813410, PMID:36271145, PMID:30097810). It binds PD-L1 at the cell surface and extends its half-life by reducing PD-L1 ubiquitination without altering transcription, a function it shares redundantly with CMTM6 (PMID:28813410); in liver cancer this stabilization is the dominant route to PD-L1 protein expression, and CMTM4 loss promotes CD8+ T-cell infiltration and sensitizes tumors to anti-PD-L1 therapy (PMID:34558800). CMTM4 is a constitutive subunit of the IL-17 receptor complex, associating with IL-17RC to mediate its glycosylation, stability, and plasma-membrane localization so that CMTM4-deficient cells cannot assemble a functional IL-17 signaling complex or respond to IL-17A (PMID:36271145), a requirement that extends to lymphatic endothelial NF-κB/chemokine output and to IL-17RC-dependent NF-κB/NOX1 signaling in gastric carcinogenesis (PMID:38754839, PMID:40432275). More broadly, CMTM4 governs the trafficking itinerary of partner receptors: it controls VE-cadherin internalization and Rab-dependent recycling to support endothelial barrier function and vascular sprouting (PMID:30097810), promotes EGFR recycling while preventing its Rab-dependent degradation to sustain EGF-driven NF-κB/mTOR/PI3K-Akt signaling (PMID:39948411), and interacts with CXCR4 to alter its glycosylation and ER-to-plasma-membrane trafficking with selective downstream effects on AKT (PMID:36044337). Across multiple cancer cell models, modulating CMTM4 tunes proliferation and migration through PI3K/Akt, ERK, and STAT signaling (PMID:32585413, PMID:31435638).

Mechanistic history

Synthesis pass · year-by-year structured walk · 14 steps
  1. 2010 Medium

    Established the first cellular consequence of CMTM4 expression, framing it as a growth regulator before any molecular partner was known.

    Evidence Overexpression of two isoforms in HeLa cells with cell-cycle and localization readouts

    PMID:20213316

    Open questions at the time
    • No molecular target or binding partner identified
    • Phenotype rests on overexpression alone
  2. 2015 Medium

    Extended the growth-suppressive role to a tumor context and linked it to a defined effector, showing CMTM4 restoration drives G2/M arrest, p21 induction, and reduced migration.

    Evidence Gain- and loss-of-function in 786-O ccRCC cells plus xenografts

    PMID:26474560

    Open questions at the time
    • Mechanism connecting CMTM4 to p21 not resolved
    • No physical partner identified
  3. 2017 High

    Resolved a direct molecular mechanism: CMTM4 binds PD-L1 and stabilizes it post-translationally by limiting ubiquitination, redundantly with CMTM6.

    Evidence Haploid genetic screen, complementation, Co-IP, ubiquitination and cycloheximide-chase assays

    PMID:28813410

    Open questions at the time
    • Structural basis of the CMTM4–PD-L1 interaction unresolved
    • Does not address non-PD-L1 client proteins
  4. 2018 High

    Showed CMTM4 acts on endocytic trafficking, controlling VE-cadherin internalization and recycling to set endothelial barrier and sprouting behavior.

    Evidence Knockdown/overexpression with Rab/EEA1 colocalization, TEER, 3D sprouting, and zebrafish morpholino

    PMID:30097810

    Open questions at the time
    • Direct CMTM4–VE-cadherin binding not demonstrated
    • Molecular step linking CMTM4 to Rab machinery unknown
  5. 2019 Medium

    Connected CMTM4 to oncogenic signaling cascades, showing it suppresses PI3K/Akt (via PAK4), ERK, and STAT3 and is itself silenced by tumor-microenvironment miRNAs.

    Evidence 3'UTR luciferase reporters, gain/loss-of-function and pathway Western blots in pancreatic and colorectal cancer cells with xenografts

    PMID:31435638 PMID:32585413

    Open questions at the time
    • Whether signaling effects are direct or downstream of receptor-stabilization roles unclear
    • No physical partner mediating these pathway changes identified
  6. 2019 High

    Defined a physiological requirement in vivo, showing CMTM4 is needed for normal spermatogenesis and fertility.

    Evidence CRISPR-Cas9 knockout mice with sperm phenotyping, IVF, acrosome assays, and quantitative testis proteomics

    PMID:30867229

    Open questions at the time
    • Molecular partner driving the testicular phenotype not identified
    • Link between CMTM4 and the 139 downregulated proteins is correlative
  7. 2021 Medium

    Demonstrated the PD-L1-stabilizing function is therapeutically actionable, with CMTM4 being the dominant PD-L1 regulator in liver cancer.

    Evidence siRNA across HCC/ICC lines, syngeneic mouse model, CD8+ T-cell profiling, anti-PD-L1 combination

    PMID:34558800

    Open questions at the time
    • Post-translational mechanism not dissected beyond prior PD-L1 model
    • Single-lab in vivo evidence
  8. 2022 High

    Identified CMTM4 as a constitutive IL-17 receptor subunit, making it essential for IL-17RC stability, glycosylation, surface localization, and IL-17A responsiveness.

    Evidence Reciprocal Co-IP, CRISPR KO human and mouse cells, psoriasis/EAE mouse models

    PMID:36271145

    Open questions at the time
    • Stoichiometry within the assembled IL-17R complex not defined
    • How CMTM4 mediates IL-17RC glycosylation mechanistically unresolved
  9. 2022 Medium

    Generalized the trafficking-regulator role to CXCR4, showing CMTM4 alters its glycosylation and slows ER-to-plasma-membrane transit with selective AKT effects.

    Evidence Co-IP, synchronized ER-release trafficking assay, glycosylation and signaling readouts, zebrafish morpholino

    PMID:36044337

    Open questions at the time
    • Surface CXCR4 levels unchanged, leaving the functional consequence partly unclear
    • Basis for AKT-selective (vs ERK) effect unknown
  10. 2024 Medium

    Extended the IL-17R partnership into lymphatic endothelium, showing CMTM4 directly binds IL-17RC to drive NF-κB-dependent chemokine secretion and modulate inflammatory drainage.

    Evidence Co-IP, knockdown NF-κB/cytokine assays, LEC-specific AAV overexpression in Prox1-CreERT2 mice

    PMID:38754839

    Open questions at the time
    • Single-lab in vivo model
    • Does not establish whether glycosylation role applies in LECs
  11. 2024 Medium

    Linked CMTM4 to intestinal homeostasis, separating a cell-intrinsic IL-17/S100a8/9 effect from microbiome-driven effects in colitis.

    Evidence KO mice, DSS colitis, cohousing microbiome transfer, RAGE inhibition, in vitro IL-17 stimulation

    PMID:38575111

    Open questions at the time
    • Causal chain between CMTM4 loss and dysbiosis not fully resolved
    • Single-lab study
  12. 2025 Medium

    Established CMTM4 as a controller of EGFR recycling that sustains pro-tumor inflammatory signaling and confers EGFR-inhibitor sensitivity upon its loss.

    Evidence Knockout with Rab-dependent EGFR trafficking/degradation assays, signaling Westerns, MDSC profiling, syngeneic tumor models, in vivo siRNA

    PMID:39948411

    Open questions at the time
    • Direct CMTM4–EGFR binding not shown
    • Which Rab steps CMTM4 acts on not pinpointed
  13. 2025 Medium

    Expanded the partner repertoire to PHB2 and to STAT2, implicating CMTM4 in STING/STAT6-driven chemokine transcription and in PD-L1-associated macrophage apoptosis through indirect signaling.

    Evidence Co-IP, ChIP-qPCR, nuclear fractionation, apoptosis flow cytometry across cervical cancer and sepsis models

    PMID:40122504 PMID:40514067

    Open questions at the time
    • PHB2 and STAT2 mechanisms each rest on single studies
    • STAT2-mediated PD-L1 effect explicitly distinguished from direct binding, leaving the connecting step open
  14. 2025 Medium

    Showed CMTM4 itself can act extracellularly via exosomes to reprogram macrophages, broadening it from an intracellular regulator to an intercellular signal.

    Evidence Exosome internalization assays, macrophage polarization, NF-κB/cytokine readouts, in vivo ovarian cancer models, drug screening

    PMID:40433989

    Open questions at the time
    • Mechanism by which exosomal CMTM4 activates macrophage NF-κB undefined
    • Single-lab study

Open questions

Synthesis pass · forward-looking unresolved questions
  • Whether CMTM4's many context-specific activities reflect a single unifying biochemical function (e.g., chaperoning/regulating glycosylation and trafficking of multiple transmembrane clients) versus distinct mechanisms per partner remains unresolved.
  • No structural model of CMTM4 or its client interactions
  • Direct binding established only for a subset of reported partners
  • Enzymatic vs scaffolding basis of glycosylation effects unknown

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0098772 molecular function regulator activity 3 GO:0060090 molecular adaptor activity 2 GO:0140313 molecular sequestering activity 2
Localization
GO:0005886 plasma membrane 4 GO:0005783 endoplasmic reticulum 1 GO:0005829 cytosol 1 GO:0031410 cytoplasmic vesicle 1
Pathway
R-HSA-162582 Signal Transduction 4 R-HSA-168256 Immune System 3 R-HSA-5653656 Vesicle-mediated transport 2 R-HSA-9609507 Protein localization 2
Partners
CD274CXCR4IL17RCPHB2
Complex memberships
IL-17 receptor complex

Evidence

Reading pass · 19 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2017 CMTM4 associates with the PD-L1 protein at the cell surface, reduces PD-L1 ubiquitination, and increases PD-L1 protein half-life without affecting PD-L1 transcription. CMTM4 shares this function with CMTM6 (demonstrated by genetic complementation in CMTM6-deficient cells), and interference with CMTM4 expression impairs PD-L1 protein expression. Haploid genetic screen, genetic complementation, co-immunoprecipitation, ubiquitination assay, protein half-life (cycloheximide chase), flow cytometry, siRNA knockdown Nature High 28813410
2022 CMTM4 is a constitutive subunit of the IL-17 receptor: it associates with IL-17 receptor subunit C (IL-17RC), mediates IL-17RC stability, glycosylation, and plasma membrane localization. CMTM4-deficient mouse and human cell lines are largely unresponsive to IL-17A due to inability to assemble the IL-17R signaling complex. CMTM4-deficient mice show severe defects in immune cell recruitment following IL-17A administration and resistance to experimental psoriasis. Co-immunoprecipitation, CRISPR/Cas9 knockout cell lines, in vivo mouse models (experimental psoriasis, EAE), IL-17A stimulation assays, glycosylation analysis Nature immunology High 36271145
2018 CMTM4 colocalizes with Rab4+ and Rab7+ endocytic vesicles and with membrane-bound and internalized VE-cadherin. CMTM4 overexpression enhances VE-cadherin internalization and promotes rapid recycling (EEA1+, Rab4+, Rab11+, Rab7+ vesicles), while CMTM4 knockdown decreases VE-cadherin internalization. CMTM4 promotes endothelial barrier function and vascular sprouting. siRNA knockdown, adenovirus-mediated overexpression, intracellular colocalization staining, 3D vascular sprouting assay, zebrafish morpholino injection, transendothelial electrical resistance (TEER) assay Angiogenesis High 30097810
2010 CMTM4-v1 and CMTM4-v2 are distributed on the cell membrane and across the cytoplasm. Overexpression of either isoform inhibits HeLa cell growth by inducing G2/M phase accumulation without inducing apoptosis. Overexpression in HeLa cells, flow cytometry (cell cycle analysis), subcellular localization (immunofluorescence) Molecules and cells Medium 20213316
2015 Restoration of CMTM4 in 786-O ccRCC cells suppresses cell growth by inducing G2/M cell cycle arrest and upregulation of p21, and inhibits cell migration. Knockdown of CMTM4 produces the opposite effects. CMTM4 overexpression inhibits tumor xenograft growth in nude mice. Overexpression and siRNA knockdown, CCK-8/cell counting, wound healing/transwell assay, flow cytometry, Western blot (p21), xenograft model Journal of experimental & clinical cancer research Medium 26474560
2019 CMTM4 suppresses PI3K/Akt signaling in pancreatic cancer cells via downregulation of PAK4. miR-5703 (from pancreatic stellate cell-derived exosomes) directly binds the 3'UTR of CMTM4 mRNA to downregulate its expression, promoting PC cell proliferation. Luciferase 3'UTR reporter assay, siRNA knockdown, CMTM4 overexpression, Western blot (PAK4, p-AKT), in vivo xenograft model Cancer letters Medium 32585413
2019 CMTM4 overexpression in colorectal cancer SW480 cells decreases phosphorylation levels of AKT, ERK1/2, and STAT3, while CMTM4 knockdown in HT29 cells elevates these. Pathway inhibitor experiments validate that these three signaling pathways contribute to CMTM4's anti-proliferative and anti-migratory effects. Overexpression and siRNA knockdown, Western blot (p-AKT, p-ERK1/2, p-STAT3), pharmacological inhibitors, proliferation and migration assays Acta biochimica et biophysica Sinica Medium 31435638
2019 CMTM4 knockout mice generated by CRISPR-Cas9 show reduced testicular daily sperm production, lower epididymal sperm motility, abnormal sperm morphology, sub-fertile phenotype, and reduced acrosome reactions. Quantitative proteomics identified 139 downregulated proteins in KO testes enriched for sperm motility and acrosome reaction functions. CRISPR-Cas9 knockout mice, Western blot, immunohistochemistry, sperm motility/morphology analysis, in vitro fertilization assay, acrosome reaction assay, quantitative mass spectrometry proteomics Molecular & cellular proteomics High 30867229
2021 CMTM4 is the major regulator of PD-L1 in liver cancer (HCC and ICC) context. CMTM4 stabilizes PD-L1 through post-translational mechanisms. In vivo, Cmtm4 suppression in immunocompetent mice inhibited HCC growth and increased CD8+ T-cell infiltration. CMTM4 depletion sensitized HCC tumors to anti-PD-L1 treatment. siRNA knockdown in multiple HCC/ICC cell lines, Western blot, in vivo syngeneic mouse model, flow cytometry (CD8+ T cells), anti-PD-L1 combination therapy Hepatology communications Medium 34558800
2022 CMTM4 interacts with CXCR4, alters its glycosylation pattern, and slows CXCR4 trafficking from the endoplasmic reticulum to the plasma membrane without affecting overall cell surface expression or CXCR4 internalization/degradation in the absence of ligand. Altered CXCR4 trafficking reduces ligand-induced CXCR4 degradation and affects AKT but not ERK1/2 activation downstream of CXCR4. Co-immunoprecipitation, synchronized ER-release trafficking assay, glycosylation analysis, CXCR4 internalization/degradation assay, Western blot (AKT, ERK1/2), zebrafish cmtm4 morpholino Molecular biology of the cell Medium 36044337
2024 CMTM4 directly binds IL-17RC in lymphatic endothelial cells (LECs). CMTM4 knockdown abrogates IL-17A plus TNF-α-induced NF-κB signaling and CXC chemokine (CXCL1/2/3/5) secretion. LEC-specific CMTM4 overexpression in Prox1-CreERT2 mice promotes neutrophil drainage and alleviates immune pathological responses. Co-immunoprecipitation (CMTM4–IL-17RC binding), siRNA knockdown, NF-κB signaling assay, cytokine/chemokine ELISA, adeno-associated virus LEC-specific overexpression in mice, in vivo inflammation/infection models Mucosal immunology Medium 38754839
2025 CMTM4 promotes EGFR recycling and prevents Rab-dependent EGFR degradation, thereby sustaining EGF signaling post-translationally. CMTM4 knockout reduces NF-κB, mTOR, and PI3K/Akt pathway activation in lung carcinoma and decreases EGF-stimulated production of inflammatory cytokines (G-CSF), leading to reduced PMN-MDSC recruitment. CMTM4 KO sensitizes tumor cells to EGFR inhibitors. CMTM4 knockout, Western blot (NF-κB, mTOR, PI3K/Akt, EGFR), EGFR recycling/degradation assay (Rab-dependent), cytokine profiling, MDSC flow cytometry, EGFR inhibitor sensitivity assay, in vivo syngeneic tumor models, siRNA-liposome in vivo delivery The EMBO journal Medium 39948411
2025 CMTM4 interacts with and stabilizes PHB2 (prohibitin 2) through post-translational modification. This CMTM4–PHB2 interaction activates the STING/TBK1/STAT6 pathway, promoting nuclear translocation of STAT6 which binds CCL2 and IL-6 promoters to upregulate their transcription, thereby driving MDSC recruitment (via CCL2/CCR2 and IL-6/GP130 axes) and immune suppression in cervical cancer. Co-immunoprecipitation (CMTM4–PHB2), chromatin immunoprecipitation (ChIP-qPCR for STAT6 at CCL2/IL-6 promoters), nuclear fractionation, Western blot (STING/TBK1/STAT6), siRNA knockdown, in vivo therapeutic models with anti-PD-1 Journal for immunotherapy of cancer Medium 40514067
2025 In sepsis, CMTM4 promotes PD-L1-mediated macrophage apoptosis by enhancing STAT2 phosphorylation rather than by directly binding PD-L1. CMTM4 inhibition reduces macrophage apoptosis. Co-immunoprecipitation (protein-protein interactions), ChIP-qPCR, Western blot (p-STAT2), flow cytometry (apoptosis), transcriptomic sequencing, in vitro macrophage model (THP-1 and C57BL/6 mice) Experimental cell research Medium 40122504
2025 Cmtm4 deletion in mice downregulates IL-17RC expression and suppresses downstream NF-κB activation and NOX1 levels in the context of H. pylori-induced gastric carcinogenesis, inhibiting GC development and precancerous lesion formation. Cmtm4 knockout mice, H. pylori infection model, Western blot (IL-17RC, NF-κB, NOX1), immunohistochemistry, DNA damage analysis Pathology international Medium 40432275
2024 Cmtm4 deficiency in mice exacerbates DSS-induced colitis and causes gut microbiome dysbiosis. CMTM4 deficiency suppresses S100a8/9 expression in vitro via the IL-17 pathway, whereas elevated S100a8/9 in vivo is attributable to microbial dysbiosis. Blocking S100a8/9 receptor RAGE reverses phenotypes associated with CMTM4 deficiency. Cmtm4 knockout mice, DSS colitis model, cohousing experiment (microbiome transfer), in vitro IL-17 stimulation, RAGE inhibitor, Western blot, 16S microbiome analysis Journal of genetics and genomics Medium 38575111
2025 Exosomal CMTM4 from ovarian cancer cells is internalized by macrophages, activates the NF-κB pathway in tumor-associated macrophages (TAMs), promotes M2 polarization, and enhances secretion of TGF-β1 and CXCL12 while upregulating ICAM1 expression to facilitate cancer metastasis. Eltrombopag was identified as a CMTM4 inhibitor in vivo. Exosome isolation/internalization assay, macrophage polarization assay, NF-κB pathway Western blot, cytokine ELISA (TGF-β1, CXCL12), ICAM1 expression analysis, CMTM4 knockdown, in vivo OC models, drug screening Advanced science Medium 40433989
2015 miR-205 inhibits apoptosis in renal HK-2 cells by directly binding to the 3'UTR of CMTM4 mRNA and inhibiting its expression; CMTM4 is identified as a pro-apoptotic target gene whose suppression mediates the anti-apoptotic effect of miR-205. Luciferase 3'UTR reporter assay, Western blot, RT-PCR, flow cytometry (apoptosis), miR-205 mimic/inhibitor overexpression Iranian journal of basic medical sciences Low 26730338
2024 CMTM4 overexpression in gastric cancer AGS cells upregulates STAT1 and enriches STAT1 signaling pathway activity (identified by TMT proteomics and confirmed by Western blot), associated with inhibition of proliferation, induction of apoptosis, and G1/S arrest. Overexpression in AGS cells, TMT quantitative proteomics, Western blot (STAT1), flow cytometry (apoptosis, cell cycle), CCK-8/clonogenic assay Journal of gastrointestinal oncology Low 39279978

Source papers

Stage 0 corpus · 31 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2017 Identification of CMTM6 and CMTM4 as PD-L1 protein regulators. Nature 575 28813410
2020 Pancreatic stellate cells derived exosomal miR-5703 promotes pancreatic cancer by downregulating CMTM4 and activating PI3K/Akt pathway. Cancer letters 80 32585413
2018 CMTM4 regulates angiogenesis by promoting cell surface recycling of VE-cadherin to endothelial adherens junctions. Angiogenesis 68 30097810
2015 CMTM4 is frequently downregulated and functions as a tumour suppressor in clear cell renal cell carcinoma. Journal of experimental & clinical cancer research : CR 52 26474560
2010 Identification and characterization of CMTM4, a novel gene with inhibitory effects on HeLa cell growth through Inducing G2/M phase accumulation. Molecules and cells 43 20213316
2021 Inhibition of CMTM4 Sensitizes Cholangiocarcinoma and Hepatocellular Carcinoma to T Cell-Mediated Antitumor Immunity Through PD-L1. Hepatology communications 31 34558800
2017 Clinical significance of CMTM4 expression in hepatocellular carcinoma. OncoTargets and therapy 28 29180877
2019 CMTM4 inhibits cell proliferation and migration via AKT, ERK1/2, and STAT3 pathway in colorectal cancer. Acta biochimica et biophysica Sinica 27 31435638
2022 CMTM4 is a subunit of the IL-17 receptor and mediates autoimmune pathology. Nature immunology 22 36271145
2021 CMTM4 regulates epithelial-mesenchymal transition and PD-L1 expression in head and neck squamous cell carcinoma. Molecular carcinogenesis 21 34061408
2019 Integrated Analyses of Phenotype and Quantitative Proteome of CMTM4 Deficient Mice Reveal Its Association with Male Fertility. Molecular & cellular proteomics : MCP 21 30867229
2025 Exosomal CMTM4 Induces Immunosuppressive Macrophages to Promote Ovarian Cancer Progression and Attenuate Anti-PD-1 Immunotherapy. Advanced science (Weinheim, Baden-Wurttemberg, Germany) 19 40433989
2022 CircCYP24A1 hampered malignant phenotype of renal cancer carcinoma through modulating CMTM-4 expression via sponging miR-421. Cell death & disease 18 35220395
2024 LECs regulate neutrophil clearance through IL-17RC/CMTM4/NF-κB axis at sites of inflammation or infection. Mucosal immunology 14 38754839
2020 Expression Analysis of Canine CMTM6 and CMTM4 as Potential Regulators of the PD-L1 Protein in Canine Cancers. Frontiers in veterinary science 13 32596272
2015 MicroRNA-205 inhibits renal cells apoptosis via targeting CMTM4. Iranian journal of basic medical sciences 13 26730338
2022 Exosomal miR-224-5p from Colorectal Cancer Cells Promotes Malignant Transformation of Human Normal Colon Epithelial Cells by Promoting Cell Proliferation through Downregulation of CMTM4. Oxidative medicine and cellular longevity 11 35814269
2020 Expression of CMTM4 shows clinical significance in lung cancer. Translational cancer research 6 35117232
2024 Cmtm4 deficiency exacerbates colitis by inducing gut dysbiosis and S100a8/9 expression. Journal of genetics and genomics = Yi chuan xue bao 5 38575111
2022 CMTM4 makes IL-17 signaling more complex. Science signaling 4 36445938
2025 Modulation of tumor inflammatory signaling and drug sensitivity by CMTM4. The EMBO journal 2 39948411
2025 Inhibiting CMTM4 reverses the immunosuppressive function of myeloid-derived suppressor cells and augments immunotherapy response in cervical cancer. Journal for immunotherapy of cancer 2 40514067
2022 MARVEL domain containing CMTM4 affects CXCR4 trafficking. Molecular biology of the cell 2 36044337
2008 [Preparation, purification and characterization of the polyclonal antibody against human CMTM4]. Xi bao yu fen zi mian yi xue za zhi = Chinese journal of cellular and molecular immunology 2 18177617
2025 Cmtm4 Deficiency Inhibits Helicobacter pylori-Induced Gastric Carcinogenesis. Pathology international 1 40432275
2024 CMTM4 inhibits gastric tumorigenesis and metastasis. Journal of gastrointestinal oncology 1 39279978
2026 Research progress of CMTM4 in the tumor immune microenvironment and immunotherapy. Frontiers in immunology 0 42254028
2025 CMTM4 promotes the motility of colon cancer cells under radiation and is associated with an unfavorable neoadjuvant chemoradiotherapy response and patient survival in rectal cancer. Oncology letters 0 39839608
2025 CMTM4 is an adhesion modulator that regulates skeletal patterning and primary mesenchyme cell migration in sea urchin embryos. Developmental biology 0 39947420
2025 CMTM4 promotes PD-L1-mediated macrophage apoptosis by enhancing STAT2 phosphorylation in sepsis. Experimental cell research 0 40122504
2025 Downregulation of CMTM4 and Its Tumor-Suppressive Role in Colorectal Cancer: Insights From Expression and Survival Analyses. Journal of surgical oncology 0 40981430

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