Demethoxycurcumin increases the sensitivity of cisplatin‑resistant non‑small lung cancer cells to cisplatin and induces apoptosis by activating the caspase signaling pathway
- Yun Chen
- Chaojin Hong
- Xiaochen Chen
- Zhiquan Qin
Affiliations: Department of Oncology, Zhejiang Provincial People's Hospital, People's Hospital of Hangzhou Medical College, Hangzhou, Zhejiang 310014, P.R. China
- Published online on: September 8, 2020 https://doi.org/10.3892/ol.2020.12072
Copyright: © Chen
et al. This is an open access article distributed under the
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Patients with non‑small cell lung cancer (NSCLC) can develop strong drug resistance following long‑term treatment with platinum‑based drugs. Increasing doses of chemotherapeutic drugs fail to obtain better results, and serious complications occur. It has been demonstrated that upregulation of excision repair cross‑complementary 1 (ERCC1) in lung cancer cells is closely associated with cell resistance to platinum‑based chemotherapy. In addition, curcumin (CMN) enhances antitumor effects in NSCLC by downregulating ERCC1. The aim of the present study was to investigate the effects of demethoxycurcumin (DMC), a curcuminoid, on the reversal of resistance of NSCLC cells in vitro and in vivo. The present study demonstrated that DMC significantly increased the sensitivity of DDP in DDP‑resistant A549 (A549/DDP) cells. The results from an MTT assay demonstrated that DMC combined with DDP significantly attenuated the proliferation of A549/DDP cells. Furthermore, DMC exhibited decreased toxicity in normal lung fibroblast MRC‑5 cells. In addition, following treatment of A549/DDP cells with a combination of DMC and DDP, the expression of ERCC1 was reduced, the protein levels of Bcl‑2 and Bax were decreased and increased, respectively, whereas caspase‑3 was activated, according to results from western blotting. Finally, DDP combined with DMC significantly attenuated A549/DDP cell‑derived tumor growth in vivo. Taken together, the findings from the present study suggested that DMC in combination with DDP may be considered as a novel combination regimen for restoring DDP sensitivity in DDP‑resistant NSCLC cells.