Tional activity, and gives rise to cell cycle arrest and apoptosis (24). MDM2 mainly mediates p53 degradation via E3 ubiquitin ligase. The overexpression or proliferation of FLMDM4 has been observed in human solid tumors and tumor cell lines. The overexpressionEXPERIMENTAL AND THERAPEUTIC MEDICINE 17: 4100-4108,Figure five. Lesogaberan In Vivo promotion of MDM4 reduces the anticancer impact of miRNA766 in colon cancer cells. Statistical evaluation of protein expression levels of (A) MDM4, (B) Bax and (C) p53 from (D) MDM4, Bax and p53 protein bands. (E) Cell development. (F) LDH activity. (G) Cell migration rate and (H) images. Magnification, x100. (I) Apoptotic price quantified from (J) flow cytometry. (K) Caspase3/9 activity levels. ##P0.01 vs. Control; P0.01 vs. miRNA-766. Control, damaging manage group; miRNA-766, overexpression of miRNA-766 group; MDM4, MDM4 and overexpression of miRNA-766 group. miR, microRNA; Bax, B-cell lymphoma 2-associated X protein.of FLMDM4 mRNA can be detected in colon cancer cells via RT-qPCR evaluation, as reported previously (24). Inside the present study, the promotion of MDM4 decreased the anticancer impact of miRNA-766 in colon cancer cells. Wang et al also demonstrated that miRNA-766 induced p53 accumulation and G2/M arrest by straight targeting MDM4 in breast cancer (25). In conclusion, the data obtained inside the present study demonstrated that miRNA-766 reduced cell development and cell migration,and promoted LDH activity, apoptotic rate and caspase-3/9 activity levels by means of MDM4/p53 in Caco2 cells (Fig. 6). These findings supply a direct link among miR766/MDM4 and human colon cancer survival rate and cell development, which offers insight in to the p53/Bax pathway. Also, these final results help the hypothesis that genetic variants can interrupt miR-766-mediated gene regulation, and this type of regulatory gene could be critical modifiers of human colon cancer danger.CHEN et al: miRNA-766 INDUCES CELL APOPTOSIS IN HUMAN COLON CANCERFigure six. miRNA766 induces cell apoptosis in human colon cancer via MDM4/p53. miRNA, microRNA; Bax, Bcell lymphoma 2associated X protein.Acknowledgements Not applicable. Funding No funding was received. Availability of data and components The analyzed information sets generated throughout the study are offered in the corresponding author on reasonable request. Authors’ contributions WC made the experiments; GC, ZL, KL, GL and YL performed the experiments; WC and GC analysed the data; and WC wrote the manuscript. Ethics approval and consent to participate The present study was approved by the Ethical Agent Will in the Second Affiliated Hospital, Shantou University Healthcare College. Patient consent for publication Not applicable. Competing interests The authors declare that they have no competing interests
EXPERIMENTAL AND THERAPEUTIC MEDICINE 18: 425-434,Downregulation of miR152 contributes to the progression of liver fibrosis by way of targeting Gli3 in vivo and in vitroLI LI, LEI ZHANG, XIONGQI ZHAO, JUN CAO, JINGFENG LI and GUANG CHU Department of Hepatobiliary Surgery, 1st People’s Hospital of Kunming City, Kunming, Yunnan 650034, P.R. China Received March 20, 2018; Accepted January 24, 2019 DOI: 10.3892/etm.2019.7595 Abstract. The Gli family is recognized to be necessary for the activation of hedgehog signalling, which participates in the pathogenesis of liver fibrosis. The aim with the present study was to identify the association involving microRNA (miR)-152 and GLI household zinc finger 3 (Gli3) and their roles in.