BACKGROUND AND OBJECTIVE: Histone deacetylase (HDAC) inhibitors represent a 
promising class of potential anticancer agents for treatment of human 
malignancies. In this study, we investigated the effect of trichostatin A (TSA), 
one such HDAC inhibitor, in combination with docetaxel (TXT), a cytotoxic 
chemotherapy agent or erlotinib, a novel molecular target therapy drug, on lung 
cancer A549 cells.
METHODS: A549 cells were treated with TXT, erlotinib alone or in combination 
with TSA, respectively. Cell viability, apoptosis, and cell cycle distribution 
were evaluated using MTT (3- (4, 5-dimethylthiazol-2-yl) -2, 
5-diphenyltetrazolium bromide) assay, Hochst33258 staining and flow cytometry. 
Moreover, immunofluorescent staining and Western blot analysis were employed to 
examine alterations of α-tubulin, heat shock protein 90 (hsp90), epidermal 
growth factor receptor (EGFR), and caspase-3 in response to the different 
exogenous stimuli.
RESULTS: Compared with single-agent treatment, co-treatment of A549 cells with 
TSA/TXT or TSA/erlotinib synergistically inhibited cell proliferation, induced 
apoptosis, and caused cell cycle delay at the G2/M transition. Treatment with 
TSA/TXT or TSA/erlotinib led to a significant increase of cleaved caspase-3 
expression, also resulting in elevated acetylation of α-tubulin or hsp90 and 
decreased expression of EGFR, which was negatively associated with the level of 
acetylated hsp90.
CONCLUSIONS: Synergistic anti-tumor effects are observed between TXT or 
erlotinib and TSA on lung cancer cells. Such combinations may provide a more 
effective strategy for treating human lung cancer.