Open AccessEffects of HAD-B1 on the proliferation of A549 cisplatin-resistant lung cancer cells
Author(s) -
Hwa Jeong Kang,
Ji Hye Park,
HwaSeung Yoo,
Yu Mi Park,
ChongKwan Cho,
InCheol Kang
Publication year - 2018
Publication title -
molecular medicine reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.727
H-Index - 56
eISSN - 1791-3004
pISSN - 1791-2997
DOI - 10.3892/mmr.2018.8702
Subject(s) - cell cycle , cisplatin , viability assay , a549 cell , apoptosis , cell growth , oncogene , cell , downregulation and upregulation , lung cancer , biology , cancer research , medicine , oncology , chemotherapy , biochemistry , gene
The present study investigated the toxicity of HangAmDan-B1 (HAD-B1) on A549-Cisplatin resistant (A549CR) cells. HAD‑B1 inhibited the growth of A549CR cells in a concentration‑dependent manner; HAD‑B1 was more effective at inhibiting A549CR cell viability compared with vehicle‑treated cells. The reduction in viability may be due to S‑phase cell cycle arrest and the induction of apoptosis in HAD‑B1‑treated cells. Cell cycle protein profile analysis of HAD‑B1‑treated A549CR cells using an InnoPharmaScreen (IPS) ProteoChip‑based antibody microarray chip indicated downregulation of signal transducer and activator of transcription 3. The activities of caspase‑3, ‑8 and ‑9 were significantly increased in HAD‑B1‑treated cells when compared with the vehicle‑treated control group. Furthermore, the HAD‑B1‑treated group exhibited similarly increased caspase levels when compared with the Afatinib‑treated group. Taken together, these observations suggest that HAD‑B1 may be a promising candidate for further research into the therapeutic management of cisplatin-resistant lung cancer.