Suppression of autophagy facilitates hydrogen gas‑mediated lung cancer cell apoptosis
- Leyuan Liu
- Zhenfeng Yan
- Yuanyuan Wang
- Jinghong Meng
- Gang Chen
Affiliations: Department of Respiration, The Third Hospital of Hebei Medical University, Shijiazhuang, Hebei 050051, P.R. China
- Published online on: August 12, 2020 https://doi.org/10.3892/ol.2020.11973
Copyright: © Liu
et al. This is an open access article distributed under the
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Commons Attribution License.
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Our previous study found that hydrogen gas (H2) could efficiently inhibit lung cancer progression; however, the underlying mechanisms still remains to be elucidated. The present study aimed to explore the roles of H2 in lung cancer cell autophagy, and reveal the effects of autophagy on H2‑mediated lung cancer cell apoptosis and the underlying mechanisms. The expression levels of proteins associated with cell apoptosis and autophagy were detected using western blot analysis. Cell autophagy was inhibited by 3‑methyladenine treatment or Beclin1 downregulation, while rapamycin was used to induce autophagy. Cell growth and apoptosis were detected using the Cell Counting Kit‑8 and flow cytometry assays, respectively. The results demonstrated that cell apoptosis and autophagy were significantly enhanced in the A549 and H1975 lung cancer cell lines treated with H2. However, autophagy enhancement weakened H2 roles in promoting cell apoptosis and vice versa. In addition, it was found that H2 treatment induced marked decreases in the protein expression levels of phosphorylated STAT3 and Bcl2, and overexpression of STAT3 abolished H2 roles in promoting cell apoptosis and autophagy. Overall, the present study revealed that H2 can promote lung cancer cell apoptosis and autophagy via inhibiting the activation of STAT3/Bcl2 signaling and suppression of autophagy can enhance H2 roles in promoting lung cancer cell apoptosis.