Home HOME General Physiology and Biophysics 2022 General Physiology and Biophysics Vol.41, No.2, p. 115–122, 2022

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Founded: 1982
ISSN 1338-4325 (online)
ISSN 0231-5882 (print)
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General Physiology and Biophysics Vol.41, No.2, p. 115–122, 2022

Title: BDH2 promotes apoptosis and autophagy of lung adenocarcinoma cells via Akt/mTOR pathway
Author: Yongli Nie, Xiong Mei, Fengjun Cao, Xueni Zhu
Abstract: Cytoprotective autophagy induces tumor cell apoptosis or autophagic programmed cell death. Autophagy and apoptosis are implicated in the pathogenesis of lung cancer, especially lung adenocarcinoma. 3-Hydroxybutyrate dehydrogenase type 2 (BDH2), a rate-limiting catalyzer in the regulation of intracellular iron metabolism and siderophore biogenesis, has been shown to be a tumor suppressor through promotion of cell apoptosis and autophagy. However, the biological role of BDH2 on lung adenocarcinoma cell apoptosis and autophagy remains unclear. Data from Western blot and qRT-PCR showed that BDH2 was down-regulated in lung adenocarcinoma cells (A549, NCI-H1975, PC9) compared to normal human lung cells (BEAS-2B). Functional assays demonstrated that pcDNA-mediated over-expression of BDH2 reduced cell viability of lung adenocarcinoma cells, and repressed the proliferation. Cell apoptosis of lung adenocarcinoma was promoted by BDH2 over-expression with up-regulation of Bax and cleaved caspase-3. Over-expression of BDH2 reduced protein expression of p62 in lung adenocarcinoma cells, enhanced LC3 and Beclin-1. Phosphorylation of AKT and mTOR in lung adenocarcinoma cells were reduced by BDH2 over-expression. In conclusion, BDH2 functioned as a tumor suppressor in lung adenocarcinoma through promotion of Akt/mTOR-mediated cell apoptosis and autophagy.
Keywords: BDH2 — Lung adenocarcinoma — Akt/mTOR — Proliferation — Apoptosis — Autophagy
Published online: 11-Apr-2022
Year: 2022, Volume: 41, Issue: 2 Page From: 115, Page To: 122
doi:10.4149/gpb_2022002


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