Related Experiment Video
Updated: Jun 13, 2025
Using Mouse Mammary Tumor Cells to Teach Core Biology Concepts: A Simple Lab Module
Published on: June 18, 2015
CMTM4 inhibits gastric tumorigenesis and metastasis
Xiurui Han1,2, Weiwei Fu1,2, Qinghua Sun1,2,3
1Department of Gastroenterology, Peking University Third Hospital, Beijing, China.
Background:
CKLF-like MARVEL transmembrane domain-containing 4 (CMTM4) is involved in immune regulation and tumor progression; however, its role in gastric cancer (GC) remains unclear. This study explored the role and mechanism of CMTM4 in GC.
Methods:
Immunohistochemistry was used to analyze CMTM4 expression in human gastric biopsied cells from patients with GC (N=23) or chronic superficial gastritis (N=23). To investigate the function of CMTM4 in GC cells, the gene CMTM4 was knocked down and overexpressed in human gastric adenocarcinoma cell line AGS. The gene CMTM4 was overexpressed in AGS cells and human gastric cell line SGC7901. Cell Counting Kit 8 (CCK-8) and cell clonogenic assays were used to analyze the proliferation of the GC cells. Flow cytometry was used to analyze the effects of CMTM4 on apoptosis and the cell cycle. Wound healing and transwell assays were used to analyze the migration and invasion of the gastric cells, respectively. The mechanism of CMTM4 in GC cells was explored using the tandem mass tags (TMTs) proteome and verified by western blot analysis.
Results:
CMTM4 expression was more downregulated in the human GC tissues than the gastritis tissues. CMTM4 overexpression significantly inhibited the proliferation, migration, and invasion of the GC cells, whereas CMTM4 knockdown enhanced gastric cell proliferation (P>0.05), migration (P>0.05), and invasion (P>0.05). Flow cytometry showed that CMTM4 promoted apoptosis and resulted in G1/S arrest in the GC cells. In addition, the proteome and western blot results showed that STAT1 was significantly upregulated, and the STAT1 signaling pathways were enriched in the GC cells overexpressing CMTM4.
Conclusions:
Our results suggest that CMTM4 plays a tumor-suppressive role in GC and may affect the growth, migration, and invasion of GC cells through the STAT1 signaling pathway. CMTM4 might have potential value as a prognosis marker and potential therapeutic target for GC therapy.
Insights
CKLF-like MARVEL transmembrane domain-containing 4 (CMTM4) acts as a tumor suppressor in gastric cancer (GC). CMTM4 inhibits GC cell proliferation, migration, and invasion, potentially via the STAT1 signaling pathway, offering a new therapeutic target.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- CKLF-like MARVEL transmembrane domain-containing 4 (CMTM4) is implicated in immune regulation and tumor progression.
- The specific role of CMTM4 in gastric cancer (GC) pathogenesis remains largely uncharacterized.
- This study aimed to elucidate the function and underlying mechanisms of CMTM4 in GC.
Purpose of the Study:
- To investigate the expression levels of CMTM4 in gastric cancer tissues.
- To determine the functional impact of CMTM4 on gastric cancer cell proliferation, apoptosis, cell cycle, migration, and invasion.
- To explore the molecular mechanism by which CMTM4 influences gastric cancer progression, focusing on the STAT1 signaling pathway.
Main Methods:
- Immunohistochemistry was employed to assess CMTM4 expression in GC and gastritis tissues.
- CMTM4 was manipulated (knockdown and overexpression) in gastric adenocarcinoma cell lines (AGS and SGC7901).
- Cell proliferation, apoptosis, cell cycle, migration, and invasion were evaluated using CCK-8, clonogenic, flow cytometry, wound healing, and Transwell assays, respectively. Proteomic analysis (TMT) and Western blotting were used to identify the mechanism.
Main Results:
- CMTM4 expression was significantly downregulated in GC tissues compared to gastritis tissues.
- Overexpression of CMTM4 suppressed GC cell proliferation, migration, and invasion, while knockdown promoted these processes.
- CMTM4 induced apoptosis and G1/S cell cycle arrest, with STAT1 upregulation observed in CMTM4-overexpressing cells, indicating STAT1 pathway enrichment.
Conclusions:
- CMTM4 exhibits tumor-suppressive properties in gastric cancer.
- CMTM4 influences GC cell growth, migration, and invasion, potentially through the STAT1 signaling pathway.
- CMTM4 presents potential as a prognostic biomarker and therapeutic target for gastric cancer.
More Related Videos
10:28Gene Regulation and Targeted Therapy in Gastric Cancer Peritoneal Metastasis: Radiological Findings from Dual Energy CT and PET/CT
Published on: January 22, 2018
19:44Enhancement of Apoptotic and Autophagic Induction by a Novel Synthetic C-1 Analogue of 7-deoxypancratistatin in Human Breast Adenocarcinoma and Neuroblastoma Cells with Tamoxifen
Published on: May 30, 2012
Related Concept Videos
02:17The Tumor Microenvironment
02:34Inhibition of Cdk Activity
02:38Mitogens and the Cell Cycle
03:03mTOR Signaling and Cancer Progression
The mTOR pathway or the...
02:30Metastasis
Epithelial-to-Mesenchymal Transition
The epithelial-to-mesenchymal transition or EMT is a developmental process commonly observed in wound healing, embryogenesis, and cancer metastasis. EMT is induced by transforming growth factor-beta (TGF-β) or receptor tyrosine kinase (RTK) ligands, which further...
01:15Drugs that Stabilize Microtubules