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[MicroRNA-30a inhibits proliferation of hepatocellular carcinoma cells via targeted regulation of forkhead-box protein A1].
Li, Y; Fu, L; Fu, X Y; Li, R H; Peng, S F.
Afiliación
  • Li Y; Health Management Center, Xiangya Hospital, Central South University, Changsha 410008, China.
  • Fu L; Department of Infectious Diseases, Hunan Key Laboratory of Viral Hepatitis, Xiangya Hospital, Central South University, Changsha 410008, China.
  • Fu XY; Department of Infectious Diseases, Hunan Key Laboratory of Viral Hepatitis, Xiangya Hospital, Central South University, Changsha 410008, China.
  • Li RH; Department of Infectious Diseases, Hunan Key Laboratory of Viral Hepatitis, Xiangya Hospital, Central South University, Changsha 410008, China.
  • Peng SF; Department of Infectious Diseases, Hunan Key Laboratory of Viral Hepatitis, Xiangya Hospital, Central South University, Changsha 410008, China.
Zhonghua Gan Zang Bing Za Zhi ; 25(9): 706-711, 2017 Sep 20.
Article en Zh | MEDLINE | ID: mdl-29108194
Objective: To investigate the expression of microRNA-30a (miR-30a) in hepatocellular carcinoma (HCC) and related molecular mechanisms in regulating HCC cell proliferation. Methods: A total of 30 pairs of HCC and adjacent tissue samples were collected, and quantitative real-time PCR and Western blot were used to measure the mRNA and protein expression of forkhead-box protein A1 (FOXA1). Methyl thiazolyl tetrazolium (MTT) assay was used to evaluate the proliferation of HCC cells, luciferase reporter gene assay was performed to verify the target relationship between miR-30a and FOXA1, and MTT assay and Western blot were used to measure the proliferation of HepG2 cells and the protein expression of FOXA1 after miR-30a transfection. The t-test was used for comparison of data between two groups, and a one-way analysis of variance was used for comparison of data between multiple groups. P < 0.05 was considered statistically significant. Results: HCC tissue had significantly lower relative expression of miR-30a than adjacent tissue (1.049 ± 0.380 vs 1.982 ± 1.013, t = 3.985, P < 0.001). At 72 hours after miR-30a overexpression, there was a significant difference in the proliferative capacity of HepG2 cells between the blank control group, the miR-30a-NC group, and the miR-30a group (0.821 ± 0.006 vs 0.816 ± 0.013 vs 0.546 ± 0.020, F = 3.396, P < 0.05), suggesting that miR-30a overexpression significantly inhibited the proliferation of HepG2 cells. FOXA1 was a target gene of miR-30a and its protein expression was negatively regulated by miR-30a, and there was a significant difference in luciferase activity between wild-type and mutant FOXA1-3'UTR vectors (1.221 ± 0.024 vs 2.658 ± 0.031, F = 6.737, P < 0.05). In HepG2 cells, miR-30a overexpression significantly inhibited the protein expression of FOXA1, and there was a significant difference in the relative expression of FOXA1 between the blank control group, the miR-30a-NC group, and the miR-30a group (1.019 ± 0.016 vs 1.022 ± 0.017 vs 0.227 ± 0.021, F = 45.43, P < 0.05). Upregulating the protein expression of FOXA1 reversed the inhibitory effect of miR-30a on the proliferation of HepG2 cells, and there was a significant difference in the proliferative capacity of HepG2 cells between the miR-30a group and the miR-30a+FOXA1 group (0.524 ± 0.023 vs 0.843 ± 0.019, t = 2.507, P < 0.05). Conclusion: MiR-30a exerts its inhibitory effect on the proliferation of HCC cells by negatively regulating the expression of FOXA1.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Carcinoma Hepatocelular / MicroARNs / Neoplasias Hepáticas Límite: Humans Idioma: Zh Revista: Zhonghua Gan Zang Bing Za Zhi Asunto de la revista: GASTROENTEROLOGIA Año: 2017 Tipo del documento: Article País de afiliación: China Pais de publicación: China

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Carcinoma Hepatocelular / MicroARNs / Neoplasias Hepáticas Límite: Humans Idioma: Zh Revista: Zhonghua Gan Zang Bing Za Zhi Asunto de la revista: GASTROENTEROLOGIA Año: 2017 Tipo del documento: Article País de afiliación: China Pais de publicación: China