Research Papers:
NUP37, a positive regulator of YAP/TEAD signaling, promotes the progression of hepatocellular carcinoma
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Abstract
Xiaoling Luo1,*, Yuting Liu3,*, Weiguang Feng2, Liu Lei3, Yemu Du3, Jinsheng Wu3 and Shaochuang Wang3
1Department of Gastroenterology, Huai’an First People’s Hospital, Nanjing Medical University, Huai’an, Jiangsu Province 223300, P. R. China
2The Fourth People’s Hospital of Huai’an, Huai’an, Jiangsu Province 223002, P. R. China
3Department of Hepatobiliary & Pancreatic Surgery, Huai’an First People’s Hospital, Nanjing Medical University, Huai’an, Jiangsu Province 223300, P. R. China
*These authors are defined as co-first author
Correspondence to:
Shaochuang Wang, email: [email protected]
Keywords: NUP37; YAP/TEAD signaling; cell growth and motility; hepatocellular carcinoma
Received: October 02, 2016 Accepted: July 24, 2017 Published: August 18, 2017
ABSTRACT
Activation of YAP/TEAD signaling is very common in the progression of HCC (Hepatocellular carcinoma). Nuclear pore complex (NPC) regulates the shuttling of proteins between cytoplasm and nucleus. Nuclear accumulation of YAP protein has been observed in the majority of HCC tissues. However, whether NPC could regulate the YAP/TEAD signaling remains unknown. In this study, it was found NUP37, the component of NPC, significantly up-regulated in HCC clinical samples and mouse model. Over-expression of NUP37 promoted the growth, migration and invasion of HCC cells, while knocking down the expression of NUP37 inhibited the growth, migration, invasion and metastasis of HCC cells and improved the survival of the mouse model. NUP37 interacted with YAP and activated YAP/TEAD signaling by enhancing the interaction between YAP and TEAD. Taken together, these data demonstrated the oncogenic roles of NUP37 in the progression of HCC and suggested that NUP37 might be a promising therapeutic target.
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