ArticleThe Journal of biological chemistry2012
Down-regulation of CMTM8 induces epithelial-to-mesenchymal transition-like changes via c-MET/extracellular signal-regulated kinase (ERK) signaling.
Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 58 citations in OpenAlex.
- Comprehensive analysis of CMTM family and immune infiltration in esophageal carcinoma.PloS one · 2025Article
- Research advances of MAL family members in tumorigenesis and tumor progression (Review).Molecular medicine reports · 2024Review
- Osteosarcoma neutrophil extracellular trap network-associated gene recurrence and metastasis model.Journal of cancer research and clinical oncology · 2024Article
- Review
- The MAL Family of Proteins: Normal Function, Expression in Cancer, and Potential Use as Cancer Biomarkers.Cancers · 2023Review
- Current Opinions on the Relationship Between CMTM Family and Hepatocellular Carcinoma.Journal of hepatocellular carcinoma · 2023Review
- A Novel 5-Methylcytosine- and Immune-Related Prognostic Signature Is a Potential Marker of Idiopathic Pulmonary Fibrosis.Computational and mathematical methods in medicine · 2022Article
- CMTM Family and Gastrointestinal Tract Cancers: A Comprehensive Review.Cancer management and research · 2022Review
- MicroRNA-582-5p promotes triple-negative breast cancer invasion and metastasis by antagonizing CMTM8.Bioengineered · 2021Article
- CMTM8 as an LPA1-associated partner mediates lysophosphatidic acid-induced pancreatic cancer metastasis.Annals of translational medicine · 2021Article
- CMTM family proteins 1-8: roles in cancer biological processes and potential clinical value.Cancer biology & medicine · 2020Review
- Down-Regulated CMTM2 Promotes Epithelial-Mesenchymal Transition in Hepatocellular Carcinoma.OncoTargets and therapy · 2020Article
- Chemokine-Like Factor-Like MARVEL Transmembrane Domain-Containing Family in Hepatocellular Carcinoma: Latest Advances.Frontiers in oncology · 2020Review
- Research Advances in CKLF-like MARVEL Transmembrane Domain-containing Family in Non-small Cell Lung Cancer.International journal of biological sciences · 2019Review
- Diffuse Gastric Cancer: A Summary of Analogous Contributing Factors for Its Molecular Pathogenicity.International journal of molecular sciences · 2018Review
- Identification of genomic aberrations associated with lymph node metastasis in diffuse-type gastric cancer.Experimental & molecular medicine · 2018Article
- Signaling pathways and mesenchymal transition in pediatric high-grade glioma.Cellular and molecular life sciences : CMLS · 2018Review
- Rab5a is overexpressed in oral cancer and promotes invasion through ERK/MMP signaling.Molecular medicine reports · 2017Article
- CMTM5 inhibits renal cancer cell growth through inducing cell-cycle arrest and apoptosis.Oncology letters · 2017Article
- miR-19a contributes to gefitinib resistance and epithelial mesenchymal transition in non-small cell lung cancer cells by targeting c-Met.Scientific reports · 2017Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
The acquisition of an invasive phenotype is a critical turning point for malignant tumor cells. CMTM8, a potential tumor suppressor, is frequently down-regulated in solid tumors, and its overexpression induces tumor cell apoptosis. Here, we identify a new role for CMTM8 in regulating tumor cell migration. Reducing CMTM8 expression in HepG2 hepatocellular carcinoma cells results in the acquisition of epithelial-to-mesenchymal transition (EMT) features, including a morphological change from organized epithelial sheets to scattered fibroblast-like shapes, reduction of the epithelial marker E-cadherin, and an increased invasive and migratory ability. These phenotypic changes are mediated in large part by the ERK-MAPK pathway, as the MEK inhibitor U0126 and shRNA-mediated knockdown of ERK2 significantly reversed these phenotypes. Hepatocyte growth factor binding to the c-MET receptor is known to induce EMT in HepG2 cells. We found that CMTM8 knockdown in HepG2 cells induced c-MET signaling and ERK activation. Inhibition of c-MET signaling with the small molecule inhibitor SU11274 or c-MET RNAi blocked the EMT-like changes following CMTM8 knockdown. CMTM8 overexpression in HepG2 cells inhibited hepatocyte growth factor-induced EMT-like morphological changes and cell motility. Down-regulation of CMTM8 also promoted an EMT-like change in MCF-10A cells, indicating a broader role for CMTM8 in regulating cellular transformation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.