Gallic acid in theabrownin suppresses cell proliferation and migration in non‑small cell lung carcinoma via autophagy inhibition
Affiliations: College of Pharmaceutical Sciences, Zhejiang Chinese Medical University, Hangzhou, Zhejiang 310053, P.R. China, Cell Resource Bank and Integrated Cell Preparation Center of Xiaoshan District, Hangzhou Regional Cell Preparation Center (Shangyu Biotechnology Co., Ltd.), Hangzhou, Zhejiang 311200, P.R. China, Department of Neurosurgery, The Wenzhou Central Hospital, Wenzhou, Zhejiang 325000, P.R. China, Department of Neurosurgery, Affiliated Hangzhou First People's Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang 310006, P.R. China, The First Affiliated Hospital, Zhejiang Chinese Medical University, Hangzhou, Zhejiang 310053, P.R. China
- Published online on: May 23, 2023 https://doi.org/10.3892/ol.2023.13880
- Article Number: 294
Copyright: © Tian et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
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The bioactive extract of green tea, theabrownin (TB), is known to exhibit pro‑apoptotic and antitumor effects on non‑small cell lung cancer (NSCLC). Gallic acid (GA) is a crucial component of TB; however, its mechanism of action in NSCLC has been rarely studied. To date, little attention has been paid to the anti‑NSCLC activity of GA. Therefore, the present study investigated the effects of GA in vivo and in vitro. Cell Counting Kit (CCK)‑8 assay, DAPI staining and flow cytometry, wound‑healing assay and western blotting were used to assess cell viability, apoptosis, migration and protein expression, respectively. In addition, a xenograft model was generated, and TUNEL assay and immunohistochemistry analysis were performed. The CCK‑8 data showed that the viability of H1299 cells was significantly inhibited by GA in a dose‑ and time‑dependent manner. DAPI staining, Annexin‑V/PI staining and wound‑healing data showed that GA exerted pro‑apoptotic and anti‑migratory effects on H1299 cells in a dose‑dependent manner. Furthermore, the results of western blotting showed that GA significantly upregulated the levels of pro‑apoptotic proteins [cleaved (c‑)PARP, c‑caspase8, c‑caspase‑9 and the ratio of γ‑H2A.X/H2A.X]. In vivo data confirmed the antitumor effect of GA through apoptosis induction in an autophagy‑dependent manner. In conclusion, the present study confirmed the anti‑proliferative, pro‑apoptotic and anti‑migratory effects of GA against NSCLC in vitro and in vivo, providing considerable evidence for its potential as a novel candidate for the treatment of NSCLC.