1. KLF2 induces the senescence of pancreatic cancer cells by cooperating with FOXO4 to upregulate p21
- Author
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Tao Min, Zhang Dexiang, Liu Houbao, Lu Pinxiang, Wang Hui, and Dai Yuedi
- Subjects
Cyclin-Dependent Kinase Inhibitor p21 ,Male ,0301 basic medicine ,Senescence ,Carcinogenesis ,Kruppel-Like Transcription Factors ,Mice, Nude ,Cell Cycle Proteins ,Biology ,medicine.disease_cause ,Cell Line ,Mice ,03 medical and health sciences ,0302 clinical medicine ,Downregulation and upregulation ,Pancreatic cancer ,medicine ,Animals ,Cells, Cultured ,Cellular Senescence ,Gene knockdown ,Forkhead Transcription Factors ,Cell Biology ,medicine.disease ,Up-Regulation ,Pancreatic Neoplasms ,030104 developmental biology ,030220 oncology & carcinogenesis ,KLF2 ,FOXO4 ,Molecular mechanism ,Cancer research ,Protein Binding - Abstract
Pancreatic cancer is one of the most common malignancies in the world. Senescence is frequently observed in the progression of pancreatic cancer. In a previous study, we showed that KLF2 inhibited the growth and migration of pancreatic cancer. However, the mechanisms are not fully understood. In this study, we showed that overexpression of KLF2 induced the senescence of pancreatic cancer cells and inhibited tumorigenesis, and knockdown of KLF2 inhibited senescence and p21 expression. In the molecular mechanism study, KLF2 was found to interact with FOXO4 and cooperated with FOXO4 to induce the expression of p21. Downregulation of p21 and FOXO4 impaired the induction of senescence by KLF2. Overall, this study revealed the functions and mechanisms of KLF2 in senescence and provided a novel explanation for the suppressive roles of KLF2 in pancreatic cancer.
- Published
- 2020