Effect of trichostatin A on E-cadherin restoration in erlotinib resistant NSCLC

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Background Richostatin A (TSA) is a nonisoform selective HDAC inhibitor, which can regulate gene expression through modulation of the status of acetylation of histone and non-histone, thus affecting cell proliferation, apoptosis and sensitivity to chemotherapy.TSA combined with erlotinib may enhance the anti-tumor effect of drugs on lung cancer cells.
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