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| MiR-92a-3p Targeting KLF4 to Promote Malignant Progression of Hepatocellular Carcinoma |
| CAI Qingshan, ZHENG Jianxing, et al |
| Tangshan Central Hospital, Hebei Tangshan 063000, China |
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Abstract Objective: To investigate the effect of microRNA-92a-3p (miR-92a-3p) on hepatocellular carcinoma (HCC) and its molecular mechanism. Methods: qRT-PCR was used to detect the expression of miR-92a-3p and Krüppel-like factor 4 (KLF4) in human HCC cell lines SMMC-7721, Bel-7402, HepG2, Hep3B, and human normal liver cell line HL-7702. SMMC-7721 and Bel-7402 cells were divided into eight groups: Inhibitor NC group, miR-92a-3p Inhibitor group, mimic NC group, miR-92a-3p mimic group, mimic NC+oe-NC group, mimic NC+oe-KLF4 group, miR-92a-3p mimic +oe-NC group, and miR-92a-3p mimic +oe-KLF4 group. qRT-PCR was used to detect the mRNA expression levels of miR-92a-3p and KLF4 in cells. Western blot was used to detect the protein expression levels of KLF4. MTT proliferation assay was used to detect cell viability. Scratch healing and Transwell invasion assays were used to detect cell migration and invasion abilities, respectively. TargetScan was used to analyze the targeting relationship between miR-92a-3p and KLF4, and the results were verified by dual luciferase assay. Results: Compared with normal cells, miR-92a-3p was highly expressed in HCC cells, and KLF4 was lowly expressed in HCC cells (P<0.05). Compared with the normal expression group, down-regulation of miR-92a-3p significantly inhibited the proliferation, migration, and invasion abilities of SMMC-7721 and Bel-7402 cells (P<0.05). The dual luciferase assay verified the existence of a targeting binding site between miR-92a-3p and KLF4. Overexpression of KLF4 was able to inhibit the proliferation, migration, and invasion of HCC cells, and inhibit the promoting effect of overexpressed miR-92a-3p on HCC cell growth, with statistical significance (P<0.05). Conclusion: miR-92a-3p can promote proliferation, migration, and invasion of HCC cells by targeting down-regulation of KLF4.
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2024, Vol. 30 
