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miR-143-3p inhibits proliferation and invasion of hepatocellular carcinoma cells by regulating its target gene FGF1
Peng, J; Wu, H. J; Zhang, H. F; Fang, S. Q; Zeng, R.
Afiliação
  • Peng, J; Zhongnan Hospital of Wuhan University. Hubei Key Laboratory of Tumor Biological Behaviors. People’s Republic of China
  • Wu, H. J; Huazhong University of Science and Technology. Tongji Medical College. Hubei Cancer Hospital. Wuhan. People’s Republic of China
  • Zhang, H. F; Huazhong University of Science and Technology. Tongji Medical College. Hubei Cancer Hospital. Wuhan. People’s Republic of China
  • Fang, S. Q; Huazhong University of Science and Technology. Tongji Medical College. Hubei Cancer Hospital. Wuhan. People’s Republic of China
  • Zeng, R; Huazhong University of Science and Technology. Tongji Medical College. Hubei Cancer Hospital. Wuhan. People’s Republic of China
Clin. transl. oncol. (Print) ; Clin. transl. oncol. (Print);23(3): 468-480, mar. 2021. graf
Article em En | IBECS | ID: ibc-220882
Biblioteca responsável: ES1.1
Localização: ES15.1 - BNCS
ABSTRACT
Purpose To explore FGF1 and miR-143-3p expression in hepatocellular carcinoma (HCC) cells and its related mechanisms. Methods Eighty-two HCC patients treated at our hospital from January 2018 to January 2019 were enrolled as Group A, while further 80 healthy people undergoing physical examinations during the same time period were enrolled as Group B. HCC cells and normal human liver cells were purchased, with HepG2 and SMMC-7721 cells transfected with pcDNA3.1-FGF1, si-FGF1, NC, miR-143-3p-inhibitor and miR-143-3p-mimics. FGF1 and miR-143-3p expression was detected by qRT-PCR. The expression of N-cadherin, vimentin, Snail, Slug, E-cadherin and γ-catenin was detected by Western Blotting (WB). Cell proliferation was detected by MTT assay. Cell invasion was detected by Transwell. Cell apoptosis was detected by flow cytometry (FCM). Results FGF1 was highly expressed but miR-143-3p was poorly expressed in HCC cells. Areas under the curves (AUCs) of the two indicators were > 0.8. The indicators were correlated with the age, gender, tumor invasion, degree of differentiation, tumor location and TNM staging of the patients. Silencing FGF1 and overexpressing miR-143-3p could promote cell apoptosis, inhibit cell growth, cell epithelial-mesenchymal transition (EMT) and the expression of N-cadherin, vimentin, Snail and Slug, and increase the expression of E-cadherin and γ-catenin. Dual luciferase reporter gene assay (DLRGA) confirmed that FGF1 and miR-143-3p had a targeted relationship. The rescue experiment showed that the proliferation, invasion and apoptosis of HepG2 and SMMC-7721 cells in the miR-143-3p-mimics+pcDNA3.1-FGF1 and miR-143-3p-inhibitor+Si-FGF1 groups were not different from those in the miR-NC group. Conclusion Inhibiting FGF1 can upregulate miR-143-3p-mediated Hedgehog signaling pathway, and affect cells’ EMT, proliferation and invasion, so FGF1 is expected to become a potential therapeutic target for HCC (AU)
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Coleções: 06-national / ES Base de dados: IBECS Assunto principal: Fator 1 de Crescimento de Fibroblastos / Carcinoma Hepatocelular / MicroRNAs / Neoplasias Hepáticas Limite: Female / Humans / Male Idioma: En Revista: Clin. transl. oncol. (Print) Ano de publicação: 2021 Tipo de documento: Article
Buscar no Google
Coleções: 06-national / ES Base de dados: IBECS Assunto principal: Fator 1 de Crescimento de Fibroblastos / Carcinoma Hepatocelular / MicroRNAs / Neoplasias Hepáticas Limite: Female / Humans / Male Idioma: En Revista: Clin. transl. oncol. (Print) Ano de publicação: 2021 Tipo de documento: Article