Research Papers:
Increased expression of calponin 2 is a positive prognostic factor in pancreatic ductal adenocarcinoma
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Abstract
Zhaoyan Qiu1,*, Yi Chu2,*, Bing Xu2,*, Qian Wang3,*, Mingzuo Jiang2, Xiaowei Li2, Gang Wang3, Pengfei Yu2, Guoxiao Liu1, Hua Wang2, Huijie Kang2, Jiayu Liu4, Yu Zhang5, Jian-Ping Jin6, Kaichun Wu2 and Jie Liang2
1Department of General Surgery, Chinese PLA General Hospital, Beijing, China
2State Key Laboratory of Cancer Biology and Institute of Digestive Diseases, Xijing Hospital, The Fourth Military Medical University, Xi’an, China
3Department of General Surgery, Tangdu Hospital, The Fourth Military Medical University, Xi’an, China
4Department of Molecular Cellular and Developmental Biology, Yale University, New Haven, CT, USA
5Department of Cardiovascular Surgery, General Hospital of Lanzhou Military Area Command, Lanzhou, China
6Department of Physiology, Wayne State University School of Medicine, Detroit, MI, USA
*These authors contributed equally to this work
Correspondence to:
Jian-Ping Jin, email: [email protected]
Kaichun Wu, email: [email protected]
Jie Liang, email: [email protected]
Keywords: calponin 2, PDAC, prognosis, immunohistochemistry, cell transfection
Received: December 01, 2016 Accepted: April 10, 2017 Published: May 09, 2017
ABSTRACT
Calponin 2 plays an important role in regulating actin cytoskeleton, which is critical for cell division and migration. Previous studies have demonstrated that calponin 2 inhibits prostate cancer cell proliferation and metastasis. However, the role of calponin 2 in pancreatic tumor growth, metastasis and patient survival remains unclear. Here, we demonstrate that the level of calponin 2 is a positive prognostic factor for patients with pancreatic ductal adenocarcinoma (PDAC). Patients with high calponin 2 expression in the tumor presented less lymph node metastasis and longer survival. Knockdown of calponin 2 facilitated pancreatic cancer cell proliferation and metastasis. Further experiments suggested that PI3K/AKT, NF-κB, Vimentin, Fibronectin, Snail and Slug were upregulated and E-cadherin was downregulated after calponin 2 was knocked down, implicating altered functions in PDAC proliferation and metastasis. In addition, we verified that calponin 2 functioned through inhibiting PI3K/AKT and NF-κB pathways. Our study suggests that the upregulation of calponin 2 in PDAC correlates to lower malignancy and presents a novel target for the development of new treatment.
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