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Deoxyshikonin inhibits cisplatin resistance of non–small‐cell lung cancer cells by repressing Akt‐mediated ABCB1 expression and function
Author(s) -
Zhang Suhong,
Wang Yi
Publication year - 2020
Publication title -
journal of biochemical and molecular toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.526
H-Index - 58
eISSN - 1099-0461
pISSN - 1095-6670
DOI - 10.1002/jbt.22560
Subject(s) - cisplatin , protein kinase b , apoptosis , viability assay , a549 cell , chemistry , cancer research , flow cytometry , cell growth , microbiology and biotechnology , biology , biochemistry , chemotherapy , genetics
Drug resistance is a large challenge for the treatment of non–small‐cell lung cancer (NSCLC). Deoxyshikonin is the naphthoquinol compound with anticancer activity. However, the role and mechanism of deoxyshikonin in cisplatin resistance of NSCLC remain poorly understood. Cell viability was assessed using 3‐(4,5‐dimethylthiazol‐2‐yl)‐2,5‐diphenyl‐tetrazolium bromide assay. Cell apoptosis was evaluated by flow cytometry and caspase‐3 activity. We found that cisplatin‐resistant A549/cis and H1299/cis cells had higher cisplatin resistance than A549 and H1299 cells, respectively. Deoxyshikonin contributed to cisplatin‐induced viability inhibition and apoptosis in A549/cis and H1299/cis cells. Moreover, deoxyshikonin inhibited phosphorylation of Akt and the expression and function of ATP‐binding cassette subfamily B member 1 (ABCB1). Activation of protein kinase B (Akt) pathway attenuated the effect of deoxyshikonin on cisplatin resistance and ABCB1 expression and function in A549/cis and H1299/cis cells. In conclusion, deoxyshikonin suppressed cisplatin resistance in cisplatin‐resistant NSCLC cells by repressing Akt signaling‐mediated ABCB1 expression.