Helicobacter pylori CagA promotes the malignant transformation of gastric mucosal epithelial cells through the dysregulation of the miR‐155/KLF4 signaling pathway

• DOI: 10.1002/mc.23025
• Publication Date: 2019-06-04T12:42:49Z
• Authors: Yang Ou; Haifeng Ren; Rongrong Zhao; Le Song; Zhengxia Liu; Wenting Xu; Yakun Liu; Siying Wang
• Keywords: CagA; KLF4

Abstract The Helicobacter pylori (H. ) cytotoxin‐associated gene A (CagA) and Krüppel‐like transcription factor (KLF4) were both closely associated with the development progression of gastric cancer (GC). However, nature interactions between CagA KLF4 in GC has not been elucidated. Therefore, we focused on CagA‐mediated promotion malignant transformation epithelial cells. Herein, first examined expression human paracarcinoma tissues or without H. infection found that was significantly decreased ‐positive cells compared ‐negative Further functional studies revealed increased could suppress promote normal Subsequently, upregulate miR‐155 further restrict downstream KLF4. More importantly, overexpression GES‐1 promoted epithelial‐mesenchymal transition eventually facilitated tumor growth vivo. Overall, identification CagA/miR‐155/KLF4 signaling pathway provided a new insight into treatment GC.