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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: BACKGROUND, METHODS, RESULTS. Meshes: Carcinoma, Hepatocellular, Cell Line, Cell Line, Tumor, Cell Proliferation, Cell Transformation, Neoplastic, Gene Expression Regulation, Neoplastic, Humans, Liver Neoplasms, MicroRNAs, Signal Transduction, Transfection, cdc25 Phosphatases.
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Does miR-675 promote the Growth of Hepatocellular Carcinoma Cells Through the Cdc25A Pathway? Context: MicroRNAs (miRNAs) have fundamental roles in tumorigenesis. MiR-675 is upregulated in hepatocellular carcinoma(HCC) cells. However, the roles of miR-675 in hepatocellular carcinogenesis are still not fully elucidated. In this study, we focus on investigating the effect and mechanism of miR-675 in proliferation of HCC cells. The cell proliferation was measured by MTT assays after transfection with miR-675 inhibitor and miR-675 mimics in HCC cells. The expression level of miR-675 was detected by real-time quantitative reverse transcription polymerase chain reaction. Protein expression of Cdc25A was measured by western blotting analysis. In MTT assays, overexpression of miR-675 promoted the proliferation of HCC cells(<0.05. at 48 hours, <0.01. at 72 hours) compared with the miR-675mimics control group. Downexpression of miR-675 inhibited the proliferation of HCC cells(<0.05. at 48 hours, <0.01. at 72 hours) compared with the miR-675inhibitor control group. In western blotting analysis, the expression level of Cdc25A was significantly increased (<0.05) after treatment with miR-675 mimics. The expression level of Cdc25A was significantly decreased (<0.05) after treatment with miR-675 inhibitor.
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Our results indicate that miR-675 promotes proliferation in human hepatocellular carcinoma cells by associating with the Cdc25A signaling pathway. Final Decision: yes