IMR Press / FBL / Volume 17 / Issue 7 / DOI: 10.2741/4069

Frontiers in Bioscience-Landmark (FBL) is published by IMR Press from Volume 26 Issue 5 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on imrpress.com as a courtesy and upon agreement with Frontiers in Bioscience.

Open Access Article

BMP2 induces PANC-1 cell invasion by MMP-2 overexpression through ROS and ERK

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1 Department of Gastroenterology, Ruijin Hospital, Shanghai Jiaotong University, Shanghai, China
2 Department of Gastroenterology, Changhai Hospital of Second Military Medical University, Shanghai, China
3 Department of Biochemistry and Molecular Biology, Shanghai Jiaotong University School of Medicine,Shanghai, China
4 Department of Gastroenterology, The First People’s Hospital, Shanghai Jiaotong University, Shanghai, China
Front. Biosci. (Landmark Ed) 2012, 17(7), 2541–2549; https://doi.org/10.2741/4069
Published: 1 June 2012
Abstract

The emerging roles of bone morphogenetic proteins (BMPs) in the initiation and progression of multiple cancers have drawn great attention in cancer research. We hypothesized that BMP2 promotes cancer metastasis by modulating MMP-2 secretion and activity through intracellular ROS regulation and ERK activation in human pancreatic cancer. Our data showed that stimulation of PANC-1 cells with BMP2 induced MMP-2 secretion and activation, associated with decreased E-cadherin expression, resulting in epithelial-to-mesenchymal transformation (EMT) and cell invasion. Blockade of ROS by the ROS scavenger, 2-MPG, abolished cell invasion, inhibited the EMT process and decreased MMP-2 expression, suggesting ROS accumulation caused an increase in MMP-2 expression in BMP2-stimulated PANC-1 cell invasion. Furthermore, treatment of PANC-1 cells with 2-MPG or ERK inhibitor PD98059 reduced the phosphorylation of ERK, resulting in attenuation of BMP2-induced cell invasion and MMP-2 activation. Taken together, these results suggest that BMP2 induces the cell invasion of PANC-1 cells by enhancing MMP-2 secretion and acting through ROS accumulation and ERK activation.

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