ABSTRACT
Objective To investigate the role and potential molecular mechanism of the radiosensitivity of esophagus cancer cells.Methods miR-141 mimics or its negative control was transfected into esophagus cancercells KYSE-150,respectively.Radiosensitivity of esophagus cancer cells was determined by CCK-8,flow cytometry and colony formation assay.The expression level of miR-141 was determined by qRT-PCR.Western blot was used to detect the expressions of proliferation-related protein Ki67 and apoptosis-related proteins Bax and Bcl-2.Results After radiation,the expression of miR-141 was decreased in KYSE-150 cells in a dose-dependent manner (t =2.57-8.96,P ＜ 0.05).Upregulation of miR-141 significantly suppressed cell proliferation and colony formation and promoted apoptosis,indicating that overexpression of miR-141 enhanced the radiosensitivity of KYSE-150 cells(t =3.24,P ＜0.05).In addition,the miR-141 mimic significantly reduced the expressions of Ki67 and Bcl-2 protein (t =6.56,8.24,P ＜ 0.01) and inhibited the expression of Bax protein compared with miR-control group (t =3.24,P ＜ 0.01).Conclusions Over-expression of miR-141 enhances the radiosensitivity of esophagus cancer cells by regulating the expressions of proliferation-related protein Ki67 and apoptosisrelated proteins Bax and Bcl-2.