Effects of HAD-B1 on the proliferation of A549 cisplatin-resistant lung cancer cells

Kang,Hwa  Jeong; Park,Ji‑Hye; Yoo,Hwa‑Seung; Park,Yu  Mi; Cho,Chong‑Kwan; Kang,In‑Cheol

doi:10.3892/mmr.2018.8702

Effects of HAD-B1 on the proliferation of A549 cisplatin-resistant lung cancer cells

Authors:
- Hwa Jeong Kang
- Ji‑Hye Park
- Hwa‑Seung Yoo
- Yu Mi Park
- Chong‑Kwan Cho
- In‑Cheol Kang
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Affiliations: Department of Biological Science, College of Life & Health Sciences and BioChip Research Center, Hoseo University, Asan‑si, Chungcheongnam‑do 336‑795, Republic of Korea, East‑West Cancer Center, Dunsan Korean Medical Hospital of Daejeon University, Daejeon 302‑869, Republic of Korea
Published online on: March 7, 2018 https://doi.org/10.3892/mmr.2018.8702
Pages: 6745-6751

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Abstract

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.

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