Weifeng Huang1, Qingsong Chen1,2, Jiangweng Dai1,3, Yuke Zhang1, Yan Yi1, Xufu Wei1, Zhongjun Wu1. 1. Department of Hepatobiliary Surgery, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China. 2. Department of Traumatology, Chongqing University Central Hospital, Chongqing, China. 3. Department of Oncology, Chengdu Fifth People's Hospital, Chengdu, China.
Abstract
BACKGROUND: microRNAs (miRNAs) have been shown to significantly contribute to the pathogenesis of various tumors, including hepatocellular carcinoma (HCC). Specifically, miR-744-5p has been shown to be associated with tumor development, but the underlying mechanism by which miR-744-5p affects HCC remains unclear. Thus, this study sought to explore the molecular mechanism governing the function of miR-744-5p in HCC. METHODS: The expression of miR-744-5p in HCC tissues/cells was detected by quantitative reverse transcription polymerase chain reaction (qRT-PCR). Colony-formation, cell-counting kit 8 (CCK-8), Transwell, and wound-healing assays were used to assess the proliferation and metastasis of HCC cells. Additionally, the interaction between miR-744-5p and transforming growth factor-beta 1 (TGF-β1) was detected using a dual-luciferase reporter and a Western-blot analysis. RESULTS: miR-744-5p expression was shown to be significantly reduced in HCC tissues and cells. The overexpression of miR-744-5p not only significantly inhibited HCC cell proliferation, but also significantly reduced epithelial-mesenchymal transition-induced invasion. A luciferase reporter assay validated the ability of miR-744-5p to directly target TGF-β1. Further, the overexpression of TGF-β1 appeared to abolish the inhibitive effect of miR-744-5p mimics on HCC development. CONCLUSIONS: As per our findings, it was revealed that miR-744-5p suppresses HCC proliferation and invasion by regulating the TGF-β1 signaling pathway and epithelial-mesenchymal-transition (EMT). 2021 Journal of Gastrointestinal Oncology. All rights reserved.
BACKGROUND: microRNAs (miRNAs) have been shown to significantly contribute to the pathogenesis of various tumors, including hepatocellular carcinoma (HCC). Specifically, miR-744-5p has been shown to be associated with tumor development, but the underlying mechanism by which miR-744-5p affects HCC remains unclear. Thus, this study sought to explore the molecular mechanism governing the function of miR-744-5p in HCC. METHODS: The expression of miR-744-5p in HCC tissues/cells was detected by quantitative reverse transcription polymerase chain reaction (qRT-PCR). Colony-formation, cell-counting kit 8 (CCK-8), Transwell, and wound-healing assays were used to assess the proliferation and metastasis of HCC cells. Additionally, the interaction between miR-744-5p and transforming growth factor-beta 1 (TGF-β1) was detected using a dual-luciferase reporter and a Western-blot analysis. RESULTS: miR-744-5p expression was shown to be significantly reduced in HCC tissues and cells. The overexpression of miR-744-5p not only significantly inhibited HCC cell proliferation, but also significantly reduced epithelial-mesenchymal transition-induced invasion. A luciferase reporter assay validated the ability of miR-744-5p to directly target TGF-β1. Further, the overexpression of TGF-β1 appeared to abolish the inhibitive effect of miR-744-5p mimics on HCC development. CONCLUSIONS: As per our findings, it was revealed that miR-744-5p suppresses HCC proliferation and invasion by regulating the TGF-β1 signaling pathway and epithelial-mesenchymal-transition (EMT). 2021 Journal of Gastrointestinal Oncology. All rights reserved.
Authors: Michael Kleemann; Helga Schneider; Kristian Unger; Philip Sander; E Marion Schneider; Pamela Fischer-Posovszky; René Handrick; Kerstin Otte Journal: Sci Rep Date: 2018-06-13 Impact factor: 4.379