〔Abstract〕 Objective To investigate the effect of cathelicidin LL-37 on the apoptosis of gastric cancer AGS cells and its molecular mechanism. Methods Gastric cancer AGS cells were treated with different concentration of LL-37 for 24 h, MTT was used to detect theactivity of cell proliferation, Annexin V-FITC/PI double staining flow cytometry was used to detect cell apoptosis, qRT-PCR method was used to detect the mRNA expression of p53, immunofluorescence method was used to detect the protein localization of p53, Western blot was used to detect the protein expression of p53 in cell nucleus and apoptosis-related proteins such as Cleaned-caspase-3, PUMA, Bcl-2 and Bax in cells; interference with p53 gene expression verified whether LL-37 induced apoptosis of gastric cancer AGS cells by activating p53 signaling. Results LL-37 dose-dependently inhibited the proliferation of gastric cancer AGS cells, elevatedthe rate of apoptosis, up-regulated the mRNA and protein expression level of p53 and promoted the nuclear translocation of p53 protein, while increased the apoptosis proteinsexpression of Cleaved-caspase-3, PUMA and Bax, decreased the anti-apoptotic proteinexpression of Bcl-2.Interference with p53 gene expression inhibited LL-37-induced apoptosis of AGS cells. Conclusion LL-37 can induce apoptosis of gastric cancer AGS cells, and its mechanism may be related to the activation of p53 expression.