Zhong-Di Xiao1, Chun-Yu Jiao2, Hai-Tao Huang2, Li-Jia He2, Jiu-Jun Zhao2, Zhao-Yang Lu3, Lian-Xin Liu3. 1. Department of Hepatic Surgery, The First Affiliated Hospital of Harbin Medical University Harbin 150001, China ; Department of General Surgery, Daqing Group Oilfield General Hospital Daqing 163001, China. 2. Department of General Surgery, Daqing Group Oilfield General Hospital Daqing 163001, China. 3. Department of Hepatic Surgery, The First Affiliated Hospital of Harbin Medical University Harbin 150001, China.
Abstract
PURPOSE: To investigate the regulatory mechanism of miR-218 in human hepatocellular carcinoma (HCC). METHODS: qPCR was used to compare the expression levels miR-218 among six hepatocellular carcinoma cell lines and normal liver tissues. After transfecting MHCC97L cells with either miR-218 mimics or miR-218 inhibitor, western blotting was used to examine the expressing patterns of cyclinD1, p21, and PTEN/AKT/PI3K signaling pathway-related proteins. MTT and colony forming assay was used to assess the capability of cell proliferation. Bioinformatic method was applied to predict the binding of miR-218 on HoxA10, and western blotting was used to examine the modulatory effect of miR-218 AND HoxA10 on PTEN/AKT/PI3K pathway in HCC. RESULTS: The expression levels of miR-218 were frequently lower in HCC cell lines than in normal liver tissues. Over-expression of miR-218 in HCC cells significantly decreased cell proliferation whereas inhibiting miR-218 promoted cancer cell proliferation. Western blotting analysis demonstrated that tumorigenesis related protein cyclin D1 and p21, as well as PTEN/AKT/PI3K signaling pathways were actively modulated by miR-218 in HCC cells. The expression of endogenous HoxA10 was also down-regulated by miR-218 over-expression, and silencing HoxA10 directly activated PTEN in HCC cells. CONCLUSION: Modulation of miR-218 actively affected HCC cancer cell development. The regulatory mechanism of miR-218 in HCC cells was acting through PTEN/AKT/PI3K pathway and possibly associated with HoxA10.
PURPOSE: To investigate the regulatory mechanism of miR-218 in humanhepatocellular carcinoma (HCC). METHODS: qPCR was used to compare the expression levels miR-218 among six hepatocellular carcinoma cell lines and normal liver tissues. After transfecting MHCC97L cells with either miR-218 mimics or miR-218 inhibitor, western blotting was used to examine the expressing patterns of cyclinD1, p21, and PTEN/AKT/PI3K signaling pathway-related proteins. MTT and colony forming assay was used to assess the capability of cell proliferation. Bioinformatic method was applied to predict the binding of miR-218 on HoxA10, and western blotting was used to examine the modulatory effect of miR-218 AND HoxA10 on PTEN/AKT/PI3K pathway in HCC. RESULTS: The expression levels of miR-218 were frequently lower in HCC cell lines than in normal liver tissues. Over-expression of miR-218 in HCC cells significantly decreased cell proliferation whereas inhibiting miR-218 promoted cancer cell proliferation. Western blotting analysis demonstrated that tumorigenesis related protein cyclin D1 and p21, as well as PTEN/AKT/PI3K signaling pathways were actively modulated by miR-218 in HCC cells. The expression of endogenous HoxA10 was also down-regulated by miR-218 over-expression, and silencing HoxA10 directly activated PTEN in HCC cells. CONCLUSION: Modulation of miR-218 actively affected HCC cancer cell development. The regulatory mechanism of miR-218 in HCC cells was acting through PTEN/AKT/PI3K pathway and possibly associated with HoxA10.
Authors: Jun Lu; Gad Getz; Eric A Miska; Ezequiel Alvarez-Saavedra; Justin Lamb; David Peck; Alejandro Sweet-Cordero; Benjamin L Ebert; Raymond H Mak; Adolfo A Ferrando; James R Downing; Tyler Jacks; H Robert Horvitz; Todd R Golub Journal: Nature Date: 2005-06-09 Impact factor: 49.962
Authors: Giovanni Vennarecci; Roberto Santoro; Mario Antonini; Cecilia Ceribelli; Andrea Laurenzi; Enrico Moroni; Mirco Burocchi; Pasquale Lepiane; Giuseppe Maria Ettorre Journal: World J Hepatol Date: 2013-03-27
Authors: Young-Bem Se; Seung Hyun Kim; Ji Young Kim; Ja Eun Kim; Yun-Sik Dho; Jin Wook Kim; Yong Hwy Kim; Hyun Goo Woo; Se-Hyuk Kim; Shin-Hyuk Kang; Hak Jae Kim; Tae Min Kim; Soon-Tae Lee; Seung Hong Choi; Sung-Hye Park; Il Han Kim; Dong Gyu Kim; Chul-Kee Park Journal: Cancer Res Treat Date: 2016-07-19 Impact factor: 4.679