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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.

Aberrant activation of beta-catenin/TCF (T-cell factor) signaling is frequently observed in the pancreatic cancer. However, the regulation of nuclear beta-catenin/TCF transcription machinery remains largely unknown. In this study, TFCP2 (transcriptional factor CP2) expression in pancreatic cancer was detected by qPCR, immunohistochemistry and western blot. Western blot, colony formation assay, migration and invasion experiment were performed to investigate the effects of TFCP2 on the growth and migration of pancreatic cancer cells. In vivo, mouse metastasis models were utilized to determine metastasis ability. Western blots were used to evaluate the related protein expression. Luciferase reporter assay was used to explore the role of TFCP2 on beta-catenin/TCF signaling. We have shown that the transcription factor TFCP2 was up-regulated in the pancreatic cancer. Over-expression of TFCP2 promoted the growth, migration, invasion and colony formation of pancreatic cancer cells, while knocking down the expression of TFCP2 inhibited the growth, migration, invasion, colony formation and metastasis of pancreatic cancer cells. The mechanism study revealed that TFCP2 interacted beta-catenin, enhanced the interaction between beta-catenin and TCF4, and activated beta-catenin/TCF signaling. Taken together, our study demonstrated the oncogenic roles of TFCP2 in pancreatic cancer, and suggested that TFCP2 might be a target for the treatment of pancreatic cancer.