Oncotarget

Research Papers:

TFCP2 activates beta-catenin/TCF signaling in the progression of pancreatic cancer

Dai Yuedi, Cai Yuankun, Zhao Jiaying, Liu Han, Wang Yueqi, Liu Houbao _ and Zhang Dexiang

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Oncotarget. 2017; 8:70538-70549. https://doi.org/10.18632/oncotarget.19741

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Abstract

Dai Yuedi1,*, Cai Yuankun2,*, Zhao Jiaying2,*, Liu Han3, Wang Yueqi3, Liu Houbao3 and Zhang Dexiang4

1Department of Medical Oncology, Cancer Hospital of Fudan University, Minhang Branch, Shanghai 200240, China

2General Surgery Department, The Fifth People’s Hospital of Shanghai, Fudan University, Shanghai 200240, China

3General Surgery Department, General Surgery Institute, Zhongshan Hospital, Fudan University, Shanghai 200032, China

4General Surgery Department, Zhongshan-Xuhui Hospital Affiliated to Fudan University, Shanghai 200031, China

*These authors have contributed equally to this work

Correspondence to:

Liu Houbao, email: [email protected]

Zhang Dexiang, email: [email protected]

Keywords: TFCP2, beta-catenin/TCF signaling, pancreatic cancer, oncogene

Received: January 02, 2017     Accepted: June 20, 2017     Published: July 31, 2017

ABSTRACT

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.


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