Open AccessSuberoylanilide hydroxamic acid overcomes erlotinib-acquired resistance via phosphatase and tensin homolog deleted on chromosome 10-mediated apoptosis in non-small cell lung cancer
Author(s) -
Pengfei Wu,
Weiwei Gao,
Cuilan Sun,
Tai Ma,
Jing Hao
Publication year - 2020
Publication title -
chinese medical journal/chinese medical journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.537
H-Index - 63
eISSN - 2542-5641
pISSN - 0366-6999
DOI - 10.1097/cm9.0000000000000823
Subject(s) - erlotinib , tensin , cancer research , erlotinib hydrochloride , pten , gefitinib , apoptosis , epidermal growth factor receptor , biology , chemistry , microbiology and biotechnology , cancer , pi3k/akt/mtor pathway , biochemistry , genetics
Epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs), such as erlotinib and gefitinib, are widely used to treat non-small cell lung cancer (NSCLC). However, acquired resistance is unavoidable, impairing the anti-tumor effects of EGFR-TKIs. It is reported that histone deacetylase (HDAC) inhibitors could enhance the anti-tumor effects of other antineoplastic agents and radiotherapy. However, whether the HDAC inhibitor suberoylanilide hydroxamic acid (SAHA) can overcome erlotinib-acquired resistance is not fully clear.