ArticleCancer cell international2024
Transmembrane protein 176B regulates amino acid metabolism through the PI3K-Akt-mTOR signaling pathway and promotes gastric cancer progression.
Article in Cancer cell international, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 9 citations in OpenAlex.
- Metabolic reprogramming in cancer: dysregulation of glucose, lipid, and amino acid pathways and therapeutic opportunities.Molecular biomedicine · 2026Review
- Integrative spatial multi-omics reveal niche-specific inflammatory signaling and differentiation hierarchies in AML.iScience · 2026Article
- Research progress on TMEM proteins in cancer progression and chemoresistance (Review).International journal of molecular medicine · 2025Review
- Lipid-Lowering Potential of Almond Hulls (Quercetin, Baicalein, and Kaempferol): Insights from Network Pharmacology and Molecular Dynamics.Current issues in molecular biology · 2025Article
- Inflammasomes in lymphocytes as therapeutic targets.Translational oncology · 2025Article
- TMEM176B inhibits ovarian cancer progression by regulating EMT via the Wnt/β-catenin signaling pathway.Journal of translational medicine · 2025Article
- Transmembrane protein 176B promotes epithelial-mesenchymal transition in colorectal cancer through inflammasome inhibition.World journal of gastrointestinal oncology · 2025Article
- Targeting Asparagine Metabolism in Solid Tumors.Nutrients · 2025Review
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundThe present study aimed to investigate the expression level, biological function, and underlying mechanism of transmembrane protein 176B (TMEM176B) in gastric cancer (GC).
methodsTMEM176B expression was detected by quantitative real-time polymerase chain reaction (qRT-PCR) and western blotting (WB). The function of TMEM176B was determined by various in vitro assays including colony formation, 5-ethynyl-2'-deoxyuridine (EdU), Transwell, and flow cytometry. Bioinformatics techniques were then used to elucidate the signaling pathways associated with TMEM176B activity. Tumor formation experiments were conducted on nude mice for in vivo validation of the preceding findings. TMEM176B expression was cross-referenced to clinicopathological parameters and survival outcomes.
resultsIt was observed that TMEM176B was overexpressed in GC cells and tissues. Targeted TMEM176B abrogation inhibited colony formation, proliferation, migration, and invasion but promoted apoptosis in GC cell lines while TMEM176B overexpression had the opposite effects. Subsequent experimental validation disclosed an association between TMEM176B and the phosphatidylinositol 3-carboxykinase (PI3K)-protein kinase B (Akt)-mammalian target of rapamycin (mTOR) signaling axis. Moreover, TMEM176B affects GC cancer progression by regulating asparagine synthetase (ASNS). The in vivo assays confirmed that TMEM176B is oncogenic and the clinical data revealed a connection between TMEM176B expression and the clinicopathological determinants of GC.
conclusionThe foregoing results suggest that TMEM176B significantly promotes the development of gastric cancer and is an independent prognostic factor of it.
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