ArticleBiochemical genetics2026
LncRNA CCAT1/miR-490-3p/VDAC1 Axis Promotes Colorectal Cancer Progression by Activating Glycolysis.
Article in Biochemical genetics, 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
To elucidate the molecular mechanism by which long non-coding RNA CCAT1 (LncRNA CCAT1) promotes colorectal cancer (CRC) progression via regulation of microRNA miR-490-3p and Voltage-Dependent Anion Channel 1 (VDAC1), thereby activating glycolysis. In vitro, LncRNA CCAT1, miR-490-3p, and VDAC1 expression in CRC cell lines (HT-29, SW620, SW480, HCT116) and normal colonic epithelial cells (NCM460) was quantified by qRT-PCR. Selected lines underwent CCAT1, miR-490-3p, or VDAC1 overexpression/knockdown. Dual-luciferase assays confirmed interactions between CCAT1 and miR-490-3p, and between miR-490-3p and VDAC1. Cell proliferation was assessed by CCK-8 and colony formation assays; glucose consumption, ATP production, and lactate secretion were measured by ELISA. In vivo, nude mice received subcutaneous xenografts of modified HT-29 cells. Tumor growth, body weight, histopathology, apoptosis, glycolysis-related gene/protein expression (VDAC1, Hexokinase 2 [HK2], Pyruvate Kinase M2 [PKM2], Glucose Transporter 2 [GLUT2]), and glucose metabolism were evaluated. CCAT1 was significantly upregulated in CRC cells. Its knockdown suppressed proliferation and glycolysis, whereas overexpression had the opposite effect. CCAT1 acted as a competing endogenous RNA for miR-490-3p, alleviating miR-490-3p-mediated repression of VDAC1, leading to VDAC1 upregulation. Overexpressing miR-490-3p or silencing VDAC1 inhibited CRC cell proliferation and glycolysis. In vivo, CCAT1 or VDAC1 knockdown reduced tumor growth and altered glycolysis-related gene/protein expression. LncRNA CCAT1 promotes CRC progression by sponging miR-490-3p to upregulate VDAC1, thereby activating glycolysis. The CCAT1/miR-490-3p/VDAC1 axis may serve as a promising diagnostic and therapeutic target in CRC.
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