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논문 기본 정보

자료유형
학술저널
저자정보
Yu, Ya-Qun (Department of Hepatobiliary Surgery, the Affiliated Hospital of Guilin Medical College) Weng, Jun (Department of Hepatobiliary Surgery, the Affiliated Hospital of Guilin Medical College) Li, Shu-Qun (Department of Hepatobiliary Surgery, the Affiliated Hospital of Guilin Medical College) Li, Bo (Department of Hepatobiliary Surgery, the Affiliated Hospital of Guilin Medical College) Lv, Jun (Department of Hepatobiliary Surgery, the Affiliated Hospital of Guilin Medical College)
저널정보
아시아태평양암예방학회 Asian Pacific journal of cancer prevention : APJCP Asian Pacific journal of cancer prevention : APJCP 제17권 제8호
발행연도
2016.1
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3,881 - 3,885 (5page)

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Background: 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. Materials and Methods: 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. Results: In MTT assays, overexpression of miR-675 promoted the proliferation of HCC cells(P<0.05. at 48 hours, P<0.01. at 72 hours) compared with the miR-675mimics control group. Downexpression of miR-675 inhibited the proliferation of HCC cells(P<0.05. at 48 hours, P<0.01. at 72 hours) compared with the miR-675inhibitor control group. In western blotting analysis, the expression level of Cdc25A was significantly increased (p<0.05) after treatment with miR-675 mimics. The expression level of Cdc25A was significantly decreased (p<0.05) after treatment with miR-675 inhibitor. Conclusions: Our results indicate that miR-675 promotes the proliferation in human hepatocellular carcinoma cells by associating with Cdc25A signaling pathway.

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