Effects and Potential Mechanisms of Trichostatin A (TSA) on the Proliferation and Apoptosis of Osteosarcoma Cell Line 143B

Abstract: This paper studied the effects of Trichostatin A (TSA) on the proliferation and apoptosis of osteosarcoma cell line143B and its potential mechanisms. 143B cells were treated with indicated doses of TSA in the presence or absence of p38 inhibitor (SB203580， 3 μmol/L) and JNK inhibitor (SP600125， 0.5 μmol/L)， and then the proliferation activity of cell line was determined with MTT assay and trypan blue staining. Cell apoptotic and cell cycle were observed by flow cytometry. The mitochondrial membrane potential detection was observed with JC-1 assay. The expression levels of Bax， Bcl-2， p38/JNK were determined by RT-PCR and Western blot. The results showed that TSA could significantly suppress the proliferation of 143B in a time- and dose-dependent manner with MTT/trypan blue staining analysis. The apoptotic rate was increased with TSA treatment， and the cell cycle arrest was observed (staying in G0/G1 and G2/M)， and the decrease of mitochondrial membrane potential detection was also visible. RT-PCR and Western blot showed that the expressions of Bax， Bcl-2 and p38/JNK were increased. p38/JNK inhibitors could reverse the effects of TSA on the expression level of Bax/Bcl-2. These data demonstrated that TSA could inhibit the proliferation of 143B cell in a time- and dose-dependent manner. TSA cloud also induce apoptosis and cell cycle arrest of 143B with different concentrations. The mechanisms of TSA induced apoptosis may attribute to the stimulation of mitochondrial apoptosis pathway by activating p38/MAPK and JNK/MAPK pathways.

CSTR: 32200.14.cjcb.2014.02.0003