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Background  Cisplatin is the standard first‐line chemotherapeutic agent for the treatment of non‐small cell lung cancer (NSCLC). However, resistance to chemotherapy has been a major obstacle in the management of NSCLC. Aldehyde dehydrogenase 1A1 (ALDH1A1) overexpression has been observed in a variety of cancers, including lung cancer. The purpose of this study was to investigate the effect of ALDH1A1 expression on cisplatin resistance and explore the mechanism responsible.    Methods  Reverse transcriptase‐PCR was applied to measure the messenger RNA expression of ALDH1A1, while Western blot assay was employed to evaluate the protein expression of  ALDH1A 1,  B ‐cell lymphoma 2,  B cl‐2‐like protein 4, phospho‐protein kinase  B  (p‐ AKT)  and  AKT . A short hairpin  RNA  was used to knockdown  ALDH1A 1 expression. A 3‐(4,5‐dimethylthiazol‐2‐yl)‐2,5‐diphenyltetrazolium bromide assay was used to determine the effect of  ALDH1A 1 decrease on cell viability. The cell apoptotic rate was tested using flow cytometry assay.    Results   ALDH1A 1 is overexpressed in cisplatin resistant cell line  A549/DDP , compared with  A 549.  ALDH1A1  depletion significantly decreased  A 549/ DDP  proliferation, increased apoptosis, and reduced cisplatin resistance. In addition, the phosphoinositide 3‐kinase  (PI 3 K)  /  AKT  pathway is activated in  A 549/ DDP , and  ALDH 1 A 1 knockdown reduced the phosphorylation level of  AKT . Moreover, the combination of  ALDH1A1 ‐short hairpin  RNA  and  PI 3 K / AKT  pathway inhibitor  LY 294002 markedly inhibited cell viability, enhanced apoptotic cell death, and increased cisplatin sensitivity.    Conclusion  These results suggest that  ALDH1A1  depletion could reverse cisplatin resistance in human lung cancer cell line  A 549/ DDP , and may act as a potential target for the treatment of lung cancers resistant to cisplatin.

Depleted aldehyde dehydrogenase 1 A 1 ( ALDH1A1 ) reverses cisplatin resistance of human lung adenocarcinoma cell A 549/ DDP