Gigantol inhibits cell proliferation and induces apoptosis by regulating DEK in non‑small cell lung cancer
- Yuxing Cai
- Yi Hao
- Hui Xu
- Kai Chen
- Baozhong Ren
Affiliations: Department of Respiratory Medicine, Baoji Center Hospital, Baoji, Shaanxi 721008, P.R. China, Department of Pediatric Surgery, Baoji Maternal and Child Health Care Hospital, Baoji, Shaanxi 721000, P.R. China, Department of Respiratory Medicine, Baoji Traditional Chinese Medicine Hospital, Baoji, Shaanxi 721001, P.R. China
- Published online on: September 17, 2021 https://doi.org/10.3892/etm.2021.10752
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Non‑small cell lung cancer (NSCLC) is a common type of cancer, with a mortality of >80% worldwide. Gigantol is a bibenzyl compound that displays anticancer activity. The aim of the present study was to determine the biological activity of gigantol in NSCLC and to elucidate the underlying molecular mechanism of its action. The expression of DEK proto‑oncogene (DEK) was measured in NSCLC tissues and cell lines by reverse transcription‑quantitative PCR (RT‑qPCR). The results suggested that DEK levels were significantly increased in NSCLC tissues and cell lines compared with adjacent non‑tumor tissues and BEAS‑2B normal bronchial epithelial cells, respectively. A549 cells were exposed to a series of gigantol concentrations (0, 25, 50 and 100 µM) and transfected with DEK small interfering RNA. The results of cell viability measured by MTT assay indicated that gigantol significantly decreased cell viability. Additionally, cell proliferation was assessed by CCK‑8 and apoptosis was measured by flow cytometry. In comparison with the control group, gigantol treatment inhibited cell proliferation and promoted apoptosis, whereas DEK knockdown increased gigantol‑induced suppression of proliferation and acceleration of apoptosis. Additionally, DEK overexpression reversed gigantol‑induced effects on proliferation and apoptosis. Moreover, compared with the control group, gigantol treatment decreased Ki‑67 and Bcl‑2 expression levels, increased Bax expression levels and inactivated the Wnt/β‑catenin signaling pathway, as assessed by RT‑qPCR and/or western blot. DEK knockdown further increased gigantol‑induced effects, but DEK overexpression reversed gigantol‑induced effects. To conclude, the results of the present study suggested that gigantol inhibited cell proliferation and induced apoptosis by decreasing Ki‑67 and Bcl‑2 expression, increasing Bax expression and activating the Wnt/β‑catenin signaling pathway by regulating DEK. The present study indicated the therapeutic potential of gigantol in patients with NSCLC. In addition, DEK may serve as a novel therapeutic target to enhance the effects of gigantol treatment.