Research Papers:
YEATS4 promotes the tumorigenesis of pancreatic cancer by activating beta-catenin/TCF signaling
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Abstract
Chen Jixiang1,*, Dang Shengchun1,*, Qu Jianguo1, Mao Zhengfa1, Fan Xin1, Wang Xuqing1, Zhang Jianxin1, Cui Lei1
1General Surgery Department, Affiliated Hospital, Jiangsu University, Zhenjiang City, Jiangsu Province, 212000 China
*These authors have contributed equally to this work
Correspondence to:
Cui Lei, email: [email protected]
Keywords: YEATS4, pancreatic cancer, beta-catenin/TCF signaling, cancer metastasis
Received: September 24, 2016 Accepted: November 23, 2016 Published: February 23, 2017
ABSTRACT
Beta-catenin/TCF signaling has been reported to promote the growth and metastasis of pancreatic cancer cells. However, the regulation for the beta-catenin/TCF transcriptional complex remains largely unknown. Here, we have found that YEATS4 is a positive regulator for Beta-catenin/TCF signaling. The expression of YEATS4 was elevated in clinical pancreatic cancer samples and pancreatic cancer mouse model. Up-regulation of YEATS4 promoted the growth, migration and invasion of pancreatic cancer cells, while knocking down the expression of YEATS4 inhibited the growth, migration, invasion and metastasis of pancreatic cancer cells. Moreover, the mechanism study revealed that YEATS4 interacted with beta-catenin and activated beta-catenin/TCF signaling. Furthermore, knocking down the expression of YEATS4 impaired the malignant transformation of normal pancreatic cells (HPDE6C7) by the oncogenic Ras. Taken together, our study demonstrated the oncogenic roles of YEATS4 in the progression of pancreatic cancer by activating beta-catenin/TCF signaling and suggested that YEATS4 might be a promising therapeutic target for pancreatic cancer.
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