Archives of biochemistry and biophysics · 2026
LINC01184 promotes hepatocellular carcinoma development via the miR-193a-3p/DCAF7 axis.
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Wang Bing, Zou Xun, Xiao Yuanchu
Аннотация
OBJECTIVE: Hepatocellular carcinoma (HCC) predominantly arises in individuals with chronic liver diseases and cirrhosis. Long non-coding RNAs (lncRNAs) have emerged as critical regulators of gene expression and play pivotal roles in cancer biology. The present study aimed to investigate the role of LINC01184 in modulating cell malignancy and xenograft tumor growth in HCC.
METHODS: LINC01184 expression in HCC cells were measured using RT-qPCR. Subcellular localization of LINC01184 was determined by nuclear-cytoplasmic fractionation assays. Cell proliferation, invasion, and migration were assessed through colony formation and Transwell assays. Protein levels of epithelial-mesenchymal transition (EMT) markers were quantitated by western blotting. The molecular interactions among LINC01184, miR-193a-3p and DCAF7 were examined using luciferase reporter and RNA immunoprecipitation (RIP) assays. In vivo tumorigenesis was evaluated by establishing xenograft mouse models.
RESULTS: LINC01184 was significantly upregulated in HCC cells. Knockdown of LINC01184 markedly impaired the proliferative, migratory, and invasive capacities of HCC cells, concomitant with the inhibiton of EMT process. In addition, LINC01184 acted as a competing endogenous RNA by binding to miR-193a-3p, thereby positively regulating DCAF7 expression. Moreover, overexpression of DCAF7 effectively reversed the repressive effects caused by LINC01184 depletion on HCC cell malignancy. In vivo experiments further demonstrated that DCAF7 overexpression rescued tumor growth suppression induced by LINC01184 knockdown or miR-193a-3p overexpression.
CONCLUSION: LINC01184 promotes malignant phenotypes and xenograft tumor progression in HCC through a regulatory axis involving miR-193a-3p and DCAF7.
METHODS: LINC01184 expression in HCC cells were measured using RT-qPCR. Subcellular localization of LINC01184 was determined by nuclear-cytoplasmic fractionation assays. Cell proliferation, invasion, and migration were assessed through colony formation and Transwell assays. Protein levels of epithelial-mesenchymal transition (EMT) markers were quantitated by western blotting. The molecular interactions among LINC01184, miR-193a-3p and DCAF7 were examined using luciferase reporter and RNA immunoprecipitation (RIP) assays. In vivo tumorigenesis was evaluated by establishing xenograft mouse models.
RESULTS: LINC01184 was significantly upregulated in HCC cells. Knockdown of LINC01184 markedly impaired the proliferative, migratory, and invasive capacities of HCC cells, concomitant with the inhibiton of EMT process. In addition, LINC01184 acted as a competing endogenous RNA by binding to miR-193a-3p, thereby positively regulating DCAF7 expression. Moreover, overexpression of DCAF7 effectively reversed the repressive effects caused by LINC01184 depletion on HCC cell malignancy. In vivo experiments further demonstrated that DCAF7 overexpression rescued tumor growth suppression induced by LINC01184 knockdown or miR-193a-3p overexpression.
CONCLUSION: LINC01184 promotes malignant phenotypes and xenograft tumor progression in HCC through a regulatory axis involving miR-193a-3p and DCAF7.