Abstract: Objective To study the effect of histone deacetylase inhibitors trichostatin A (TSA) and LBH589 on the growth of
human renal cell carcinoma OS-RC-2 cells in vitro and explore the underlying molecular mechanism. Methods OS-RC-2 cells
were treated with LBH589 or TSA with or without SP600125 pretreatment, and the cell viability was measured by MTT assay.
The changes of cell cycle distribution and apoptosis of OS-RC-2 cells were examined by flow cytometry, and the expressions of
c-Jun, p-c-Jun, Bcl-2, and Bax were quantified by Western blotting. Results TSA and LBH589 both inhibited the growth of
OS-RC-2 cells in a dose- and time-dependent manner. TSA at 1 μnmol/L and LBH589 at 50 nmol/L caused obvious cell cycle
arrest in G2/M phase and cell apoptosis, and significantly increased the protein levels of phosphorylated c-Jun. TSA treatment
obviously increased Bax expression but decreased Bcl2 expression in the cells. The growth inhibitory effect of TSA was
attenuated by the JNK inhibitor SP600125 in OS-RC-2 cells. TSA-induced phosphorylation of c-Jun and Bax upregulation was
partially counteracted by SP600125. Conclusion TSA and LBH589 can cause cell cycle arrest and induce apoptosis in OS-RC-2
cells, in which process P-JNK pathway plays an important role.