Research Papers:

Periostin promotes tumor angiogenesis in pancreatic cancer via Erk/VEGF signaling

Yang Liu _, Fan Li, Feng Gao, Lingxi Xing, Peng Qin, Xingxin Liang, Jiajie Zhang, Xiaohui Qiao, Lizhou Lin, Qian Zhao and Lianfang Du

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Oncotarget. 2016; 7:40148-40159. https://doi.org/10.18632/oncotarget.9512

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Yang Liu1,*, Fan Li1,*, Feng Gao1, Lingxi Xing1, Peng Qin2, Xingxin Liang1, Jiajie Zhang1, Xiaohui Qiao1, Lizhou Lin1, Qian Zhao3, Lianfang Du1

1Department of Ultrasound, Shanghai General Hospital, Shanghai Jiaotong University School of Medicine, Shanghai 200080, China

2Department of Instrument Science and Engineering, Shanghai Jiao Tong University, Shanghai 200240, China

3Department of Pathophysiology, Key Laboratory of Cell Differentiation and Apoptosis and National Ministry of Education, Shanghai Jiaotong University School of Medicine, Shanghai 200025, China

*These authors have contributed equally to this work

Correspondence to:

Lianfang Du, email: [email protected]

Qian Zhao, email: [email protected]

Keywords: periostin, pancreatic cancer, angiogenesis, Erk, VEGF

Received: February 19, 2016     Accepted: April 26, 2016     Published: May 20, 2016


Pancreatic cancer (PaC) consists of a bulk of stroma cells which contribute to tumor progression by releasing angiogenic factors. Recent studies have found that periostin (POSTN) is closely associate with the metastatic potential and prognosis of PaC. The purpose of this study is to determine the role of POSTN in tumor angiogenesis and explore the precise mechanisms. In this study, we used lentiviral shRNA and human recombinant POSTN protein (rPOSTN) to negatively and positively regulate POSTN expression in vitro. We found that increased POSTN expression promoted the tubule formation dependent on human umbilical vein endothelial cells (HUVECs). Moreover, knockdown of POSTN in PaC cells reduced tumor growth and VEGF expression in vivo. In accordance with these observations, we found that Erk phosphorylation and its downstream VEGF expression were upregulated achieved in rPOSTN-treated groups, opposing results were obversed in POSTN-slienced group. Meanwhile, Erk inhibitor SCH772984 significantly decreased VEGF expression as well as tubule formation of HUVECs in rPOSTN-treated PaC cells. Taken together, these findings suggest that POSTN promotes tumor angiogenesis via Erk/VEGF signaling in PaC and POSTN may be a new target for cancer anti-vascular treatment.

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