Empagliflozin promotes autophagy and apoptosis in A549 lung cancer cells
Abstract
Purpose: The objective of the present study is to investigate antiproliferative effects of empagliflozin (EMPA) and to determine whether it induces autophagic cell death in lung cancer cells. Materials and Methods: A549 lung cancer cells were treated with increasing concentrations of EMPA, and cell viability was assessed by MTT assay. Autophagy and apoptosis related markers (LC3B, caspase-3, caspase-9) were examined by western blotting. Clonogenic assays were performed following treatment with EMPA alone or in combination with everolimus (RAD001) or hydroxychloroquine (HCQ). Results: EMPA significantly reduced A549 cell viability in a dose-dependent manner. The IC50 values were 54.11 µM at 24 h and 109.6 µM at 48 h. EMPA also markedly decreased clonogenic capacity by 66% and induced morphological alterations. In addition, the expression levels of LC3B and cleaved caspase-3 were increased. Our findings demonstrate that EMPA activates autophagy and triggers caspase-3 dependent apoptotic cell death. Conclusion: Empagliflozin exerts significant antiproliferative activity in lung cancer cells through the induction of autophagy and caspase-3 mediated apoptosis. Its ability to modulate autophagic and apoptotic pathways suggests that EMPA may represent a potential candidate for future combination based therapeutic strategies in lung cancer. Further mechanistic investigations and in vivo studies are warranted to validate these findings.
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