p21 promotes gemcitabine tolerance in A549 cells by inhibiting DNA damage and altering the cell cycle

Gemcitabine is one of the most widely used chemotherapy drugs for advanced malignant tumors, including non‑small cell lung cancer. However, clinical efficacy gemcitabine limited due to drug resistance. The aim present study was investigate role p21 in gemcitabine‑resistant A549 (A549/G+) cancer cells. IC50 values were determined using a Cell Counting Kit‑8 (CCK‑8) assay. mRNA and protein expression levels genes measured by reverse transcription‑quantitative PCR western blotting, respectively. cycle distribution apoptosis rate analyzed flow cytometry. DNA damage cells evaluated single‑cell gel electrophoresis. results blot analysis CCK‑8 assay demonstrated that higher A549/G+ than gemcitabine‑sensitive Knockdown sensitized these (with decreasing from 84.2 26.7 µM). revealed different changes treated with same concentration gemcitabine, decreased shown promote G1 arrest. comet resulted accumulation unrepaired double‑strand breaks (DSBs) induction gemcitabine. knockout promotes DSB accumulation, accompanied These indicated involved regulating response