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Gastric cancer is the third leading cause of cancer death worldwide. In this study, we tried to clarify the function of  KLF5  in gastric cancer. Copy number variation (CNV) and the expression of  KLF5  were interrogated in public datasets. The clinical significance of  KLF5  amplification and gene expression in gastric cancer were evaluated. The function of  KLF5  in cell proliferation was studied in gastric cancer cell lines and organoids. We found that  KLF5  amplification mainly occurred in the chromosome instable tumors (CIN) and was significantly associated with  TP53  mutation. In addition, higher  KLF5  expression correlated with more locally invasive gastric cancer and higher T stage. Next, a  KLF5  gene expression signature was curated. The genes in the signature were involved in cell development, cell cycle regulation, cell death, suggesting potential roles played by  KLF5 . Functional studies using siRNAs revealed that  KLF5  was essential for the proliferation of gastric cancer cells. Finally, using gastric organoid models, we revealed that the proliferation of organoids was significantly inhibited after the down regulation of  KLF5 . Our study revealed that  KLF5  was amplified and over-expressed in gastric cancer, and it may play an oncogene-like role in gastric cancer by supporting cell proliferation.

KLF5 Is Activated by Gene Amplification in Gastric Cancer and Is Essential for Gastric Cell Proliferation