ArticleFrontiers in immunology2026
TMEM160 promotes hepatocellular carcinoma cell proliferation, invasion, and immune evasion by regulating the VEGFA/PI3K/AKT signaling axis.
Article in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Objective: Hepatocellular carcinoma (HCC) remains a major cause of cancer-related mortality, and TMEM160 is potentially involved in tumor progression and immune escape. This study aimed to determine the expression pattern and clinical relevance of TMEM160 in HCC. Methods: TMEM160 expression was analyzed in public HCC cohorts and validated in 76 paired HCC tissues and adjacent non-tumor tissues. Survival associations were assessed using Kaplan-Meier analysis. TMEM160 was silenced in Huh7 and Hep3B cells and overexpressed in SNU449 cells, followed by assays of proliferation, invasion, and endothelial tube formation using HUVECs conditioned medium. PD-L1 protein expression was detected by Western blotting. HCC cells were co-cultured with PBMCs, followed by ELISA detection of IFN-γ, IL-2, IL-10, and TGF-β secretion and flow cytometric analysis of CD8 Results: TMEM160 was increased in HCC tissues and HCC cells, and high TMEM160 expression was associated with poorer overall survival. TMEM160 knockdown reduced HCC cell viability, invasion, HUVEC tube formation with decreased VEGFA expression. TMEM160 knockdown also decreased PD-L1 protein levels in HCC cells. TMEM160 modulation was accompanied by concordant changes in PI3K/AKT phosphorylation, and VEGFA overexpression increased PI3K/AKT phosphorylation and partially rescued inhibitory phenotypes caused by TMEM160 silencing. Conclusion: These findings supported that TMEM160 might affect VEGFA-associated PI3K/AKT signaling to promote malignant phenotypes in HCC, suggesting TMEM160 as a candidate molecular target for further investigation.
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