Dual roles of yes-associated protein (YAP) in colorectal cancer
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Chunlin Ou1,2,3, Zhenqiang Sun1,2,4,5, Shen Li1,2, Guiyuan Li1,2, Xiayu Li3,* and Jian Ma1,2,3,*
1Hunan Cancer Hospital and the Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha, Hunan 410013, China
2Key Laboratory of Carcinogenesis and Cancer Invasion of the Chinese Ministry of Education, Cancer Research Institute, Central South University, Changsha, Hunan 410078, China
3Hunan Key Laboratory of Nonresolving Inflammation and Cancer, The Third Xiangya Hospital, Central South University, Changsha, Hunan 410013, China
4Department of Anorectal Surgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan 450052, China
5Department of Gastrointestinal Surgery, Tumor Hospital of Xinjiang Medical University, Urumqi, Xinjiang 830011, China
*These authors contributed equally to this work
Jian Ma, email: [email protected]
Xiayu Li, email: [email protected]
Keywords: colorectal cancer, Yes-associated protein, tumour biomarker, stemness maintenance, inflammation
Received: July 07, 2017 Accepted: July 30, 2017 Published: August 11, 2017
Yes-associated protein (YAP) is a downstream effector molecule of a newly emerging tumour suppressor pathway called the Hippo pathway. YAP is a transcriptional co-activator and mis-expressed in various cancers, including colorectal cancer (CRC). Accumulating studies show that the high expression of nuclear YAP is linked with tumour progression and decreased survival. Nuclear YAP can interact with other transcription factors to promote cancer cell proliferation, apoptosis, metastasis and maintenance of stemness. Therefore, YAP has the potential to be a tumour biomarker or therapeutic target for CRC. However, recently, a number of studies have supported a contradictory role for YAP as a tumour suppressor, demonstrating inhibition of the tumorigenesis of CRC, involvement in promoting cell apoptosis, and inhibiting the maintenance of intestinal stem cells and inflammatory activity. In these studies, high expression of YAP was highly correlated with worse survival in CRC. In this review, we will comprehensively summarize and analyse these paradoxical reports, and discuss both the oncogenic and tumour suppressor functions of YAP in the differential status of CRC progression. Further investigation into the mechanisms responsible for the dual function of YAP will be of great value in the prevention, early diagnosis, and therapy of CRC.
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