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miR-143-3p inhibits proliferation and invasion of hepatocellular carcinoma cells by regulating its target gene FGF1.
Clin Transl Oncol. 2020 Jul 02 [Online ahead of print]CT

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.

Authors+Show Affiliations

Hubei Key Laboratory of Tumor Biological Behaviors, Zhongnan Hospital of Wuhan University, Wuhan, 430071, People's Republic of China. Department of Radiation and Medical Oncology, Zhongnan Hospital of Wuhan University, Wuhan, 430071, People's Republic of China. Hubei Cancer Clinical Study Center, Zhongnan Hospital of Wuhan University, Wuhan, 430071, People's Republic of China.Department of Gynecologic Oncology, Hubei Cancer Hospital, Tongji Medical College, Huazhong University of Science and Technology, No. 117 Zhuodaoquan South Road, Wuhan, 430079, People's Republic of China.Department of Gynecologic Oncology, Hubei Cancer Hospital, Tongji Medical College, Huazhong University of Science and Technology, No. 117 Zhuodaoquan South Road, Wuhan, 430079, People's Republic of China.Department of Gynecologic Oncology, Hubei Cancer Hospital, Tongji Medical College, Huazhong University of Science and Technology, No. 117 Zhuodaoquan South Road, Wuhan, 430079, People's Republic of China.Department of Gynecologic Oncology, Hubei Cancer Hospital, Tongji Medical College, Huazhong University of Science and Technology, No. 117 Zhuodaoquan South Road, Wuhan, 430079, People's Republic of China. rpz5s5@163.com.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

32617870

Citation

Peng, J, et al. "MiR-143-3p Inhibits Proliferation and Invasion of Hepatocellular Carcinoma Cells By Regulating Its Target Gene FGF1." Clinical & Translational Oncology : Official Publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico, 2020.
Peng J, Wu HJ, Zhang HF, et al. MiR-143-3p inhibits proliferation and invasion of hepatocellular carcinoma cells by regulating its target gene FGF1. Clin Transl Oncol. 2020.
Peng, J., Wu, H. J., Zhang, H. F., Fang, S. Q., & Zeng, R. (2020). MiR-143-3p inhibits proliferation and invasion of hepatocellular carcinoma cells by regulating its target gene FGF1. Clinical & Translational Oncology : Official Publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico. https://doi.org/10.1007/s12094-020-02440-5
Peng J, et al. MiR-143-3p Inhibits Proliferation and Invasion of Hepatocellular Carcinoma Cells By Regulating Its Target Gene FGF1. Clin Transl Oncol. 2020 Jul 2; PubMed PMID: 32617870.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - miR-143-3p inhibits proliferation and invasion of hepatocellular carcinoma cells by regulating its target gene FGF1. AU - Peng,J, AU - Wu,H J, AU - Zhang,H F, AU - Fang,S Q, AU - Zeng,R, Y1 - 2020/07/02/ PY - 2020/04/09/received PY - 2020/06/19/accepted PY - 2020/7/4/entrez KW - Biological functions KW - Diagnosis KW - FGF1 KW - Hepatocellular carcinoma KW - Prognosis JF - Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico JO - Clin Transl Oncol N2 - 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. SN - 1699-3055 UR - https://www.unboundmedicine.com/medline/citation/32617870/miR-143-3p_inhibits_proliferation_and_invasion_of_hepatocellular_carcinoma_cells_by_regulating_its_target_gene_FGF1 L2 - https://dx.doi.org/10.1007/s12094-020-02440-5 DB - PRIME DP - Unbound Medicine ER -
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