MiRNA153 Reduces Effects of Chemotherapeutic Agents or Small Molecular Kinase Inhibitor in XXXX Cells.

@entity0 @entity5 @entity2857 @entity1311 @entity2879 @entity98 @entity4012 @entity983 @entity157
UNASSIGNED: MicroRNA-153 (miR-153) is considered to be a @entity5 regulator. Silencing of miR-153 expression induced apoptosis in @entity0 cells. Data on mechanism suggest that up-regulation of miR-153 level promotes cell proliferation via the down regulation the expression of @entity983 or @entity4012 , which attenuates the proliferation of cancerous cells. This study aims to identify the effect of miR-153 on the activity of chemotherapeutic Agents and targeted agents in @entity157 cells and to investigate the mechanisms involved. @entity98 , soft agar, trans-well and flow cytometry assays were performed to examine whether miR-153 down-regulated the activity of the chemotherapeutic and targeted drugs, @entity2857 , @entity2879 and @entity1311 in HepG2 cells. The rate of proliferation inhibition, relative survival rates and IC50 values of each drug were calculated. Western blot and luciferase assays were performed to assess whether miR-153 modulates the expression of important genes related to cell proliferation, apoptosis and survival. Results showed that miR-153 attenuated the effect of @entity2879 , @entity1311 and @entity2857 on HepG2 cells, the IC50 value increased from 0.25  0.01 mol/L to 1.02  0.14 mol/L, 0.05  0.01 mol/L to 0.14  0.02 mol/L and from 1.09  0.15 mol/L to 5.18  0.99 mol/L, respectively. In addition, miR-153 also reduced the effect of these drugs on SMMC-7721, BEL-7402 or Hu7 cell; and it also reduced the effects of @entity2857 , @entity2879 and @entity1311 on anchor-independent growth of HepG2 cells. Over-expression of miR-153 down-regulated the activity of @entity2879 and @entity1311 on cell cycle arrest of HepG2 cells and the effect of @entity2857 on the invasion and migration of HepG2 cells. Furthermore, overexpression of miR-153 also enhanced growth of HepG2, MHCC-97H, MHCC-97 L and L-02 cells. These results show that overexpression of miR-153 protects HepG2 cells against the effects of these chemotherapeutic drugs via multiple mechanisms, and miR-153 may be a novel target for @entity157 in future diagnostic and therapeutic interventions.
