J-T Wang1, Z-H Wang. 1. Department of Hepatobiliary Surgery, Yantai Yantaishan Hospital, Yantai, China. jtxj37@163.com.
Abstract
OBJECTIVE: This study aims at exploring the regulatory effects of miR-193a-5p on hepatocellular carcinoma (HCC). It might provide new insight into the improvement of clinical treatment of HCC. PATIENTS AND METHODS: A total of 50 HCC patients who did not receive any tumor treatments were recruited, and 50 paired tumor tissues and adjacent non-tumor tissues were obtained. Quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) was performed to validate the expression and significance of miR-193a-5p in HCC tumor tissues, adjacent non-tumor tissues and cell lines. Binding-site of the target gene of miR-193a-5p was predicted by bioinformatics and further verified by Dual-Luciferase reporter gene assay and Western blotting (WB) assay. To investigate the potential role of miR-193a-5p in HCC development, cell counting kit-8 (CCK-8) assay was performed to study the proliferation and viability capacities. Flow cytometric analyses were adopted to test the cell cycle distribution and quantify the apoptotic cell proportion. RESULTS: MiR-193a-5p expression was specifically up-regulated in HCC tissues and cell lines compared with paired adjacent non-tumor tissues and normal liver cell lines (HL-7702) respectively. BMF was considered as a downstream gene of miR-193a-5p, which was further proofed in Dual-Luciferase reporter gene assay and Western blot assays. In vitro experiments showed that miR-193a-5p overexpression could accelerate the proliferation, facilitate the G1/S transition and suppress the apoptosis of HCC cells. However, BMF overexpression could reverse the effects of miR-193a-5p on the cellular functions of HCC cells. CONCLUSIONS: This finding suggested that miR-193a-5p is strongly up-regulated in HCC. MiR-193a-5p promoted the abnormal proliferation of HCC cells and limited their apoptosis by targeting the downstream gene BMF. Thus, the miR-193a-5p/BMF axis might be a novel regulatory pathway of apoptosis which could be potential therapeutic sites in HCC treatment.
OBJECTIVE: This study aims at exploring the regulatory effects of miR-193a-5p on hepatocellular carcinoma (HCC). It might provide new insight into the improvement of clinical treatment of HCC. PATIENTS AND METHODS: A total of 50 HCC patients who did not receive any tumor treatments were recruited, and 50 paired tumor tissues and adjacent non-tumor tissues were obtained. Quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) was performed to validate the expression and significance of miR-193a-5p in HCC tumor tissues, adjacent non-tumor tissues and cell lines. Binding-site of the target gene of miR-193a-5p was predicted by bioinformatics and further verified by Dual-Luciferase reporter gene assay and Western blotting (WB) assay. To investigate the potential role of miR-193a-5p in HCC development, cell counting kit-8 (CCK-8) assay was performed to study the proliferation and viability capacities. Flow cytometric analyses were adopted to test the cell cycle distribution and quantify the apoptotic cell proportion. RESULTS: MiR-193a-5p expression was specifically up-regulated in HCC tissues and cell lines compared with paired adjacent non-tumor tissues and normal liver cell lines (HL-7702) respectively. BMF was considered as a downstream gene of miR-193a-5p, which was further proofed in Dual-Luciferase reporter gene assay and Western blot assays. In vitro experiments showed that miR-193a-5p overexpression could accelerate the proliferation, facilitate the G1/S transition and suppress the apoptosis of HCC cells. However, BMF overexpression could reverse the effects of miR-193a-5p on the cellular functions of HCC cells. CONCLUSIONS: This finding suggested that miR-193a-5p is strongly up-regulated in HCC. MiR-193a-5p promoted the abnormal proliferation of HCC cells and limited their apoptosis by targeting the downstream gene BMF. Thus, the miR-193a-5p/BMF axis might be a novel regulatory pathway of apoptosis which could be potential therapeutic sites in HCC treatment.
Authors: Yu Jin; Ye Shen Wong; Brian K P Goh; Chung Yip Chan; Peng Chung Cheow; Pierce K H Chow; Tony K H Lim; George B B Goh; Thinesh Lee Krishnamoorthy; Rajneesh Kumar; Tze Pin Ng; Samuel S Chong; Hwee Huang Tan; Alexander Y F Chung; London Lucien P J Ooi; Jason P E Chang; Chee Kiat Tan; Caroline G L Lee Journal: Sci Rep Date: 2019-07-18 Impact factor: 4.379
Authors: Raphael Mohr; Burcin Özdirik; Joeri Lambrecht; Münevver Demir; Johannes Eschrich; Lukas Geisler; Teresa Hellberg; Sven H Loosen; Tom Luedde; Frank Tacke; Linda Hammerich; Christoph Roderburg Journal: Int J Mol Sci Date: 2021-02-02 Impact factor: 5.923