Guangyu Qian1, Xiaoyan Jin2, Louwei Zhang1. 1. Department of Hepatobiliary Surgery, Zhuji Affiliated Hospital of Shaoxing University, Zhuji, China. 2. Department of Surgical Oncology, Taizhou Municipal Hospital, Taizhou, China.
Abstract
Background: Abnormal long noncoding RNA FOXF1 adjacent noncoding developmental regulatory RNA (FENDRR) expression has been discovered in multiple human cancers pathogenesis, but its role in hepatocellular carcinoma (HCC) cells is rarely reported. Its effects on HCC cells are covered in this study. Materials and Methods: MiR-362-5p and NPR3 expressions in HCC tissues and cell were detected by quantitative real-time polymerase chain reaction and Western blot as needed. Cell viability and apoptosis were detected by MTT assay and flow cytometry, respectively. Target gene and potential binding sites of FENDRR, miR-362-5p, and NPR3 were predicted and confirmed by TargetScan and Starbase, and dual-luciferase reporter assay. Results: FENDRR expression was downregulated while miR-362-5p expression was upregulated in HCC tissues and cells. FENDRR upregulation inhibited HCC cells viability yet induced apoptosis, which was reversed by miR-362-5p. In addition, miR-362-5p resulted in p38-mitogen-activated protein kinase (MAPK) pathway activation and NPR3 expression decrease in HCC cells, which was reversed by FENDRR. Conclusion: FENDRR inhibited HCC cells viability yet promoted apoptosis by targeting miR-362-5p by promoting NPR3 and deactivating p38-MAPK pathway, thus exerting its anticarcinogenic effects in HCC cells.
Background: Abnormal long noncoding RNA FOXF1 adjacent noncoding developmental regulatory RNA (FENDRR) expression has been discovered in multiple humancancers pathogenesis, but its role in hepatocellular carcinoma (HCC) cells is rarely reported. Its effects on HCC cells are covered in this study. Materials and Methods:MiR-362-5p and NPR3 expressions in HCC tissues and cell were detected by quantitative real-time polymerase chain reaction and Western blot as needed. Cell viability and apoptosis were detected by MTT assay and flow cytometry, respectively. Target gene and potential binding sites of FENDRR, miR-362-5p, and NPR3 were predicted and confirmed by TargetScan and Starbase, and dual-luciferase reporter assay. Results:FENDRR expression was downregulated while miR-362-5p expression was upregulated in HCC tissues and cells. FENDRR upregulation inhibited HCC cells viability yet induced apoptosis, which was reversed by miR-362-5p. In addition, miR-362-5p resulted in p38-mitogen-activated protein kinase (MAPK) pathway activation and NPR3 expression decrease in HCC cells, which was reversed by FENDRR. Conclusion:FENDRR inhibited HCC cells viability yet promoted apoptosis by targeting miR-362-5p by promoting NPR3 and deactivating p38-MAPK pathway, thus exerting its anticarcinogenic effects in HCC cells.