Oncotarget

Research Papers:

p62/IMP2 stimulates cell migration and reduces cell adhesion in breast cancer

Yang Li _, Giulio Francia and Jian-Ying Zhang

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Oncotarget. 2015; 6:32656-32668. https://doi.org/10.18632/oncotarget.5328

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Abstract

Yang Li1, Giulio Francia1, Jian-Ying Zhang1

1Department of Biological Sciences & NIH-Sponsored Border Biomedical Research Center, The University of Texas at El Paso, El Paso, TX 79968, USA

Correspondence to:

Jian-Ying Zhang, e-mail: jzhang@utep.edu

Giulio Francia, e-mail: gfrancia@utep.edu

Keywords: breast cancer, IGF2 mRNA binding protein 2, cell migration, cell adhesion, extracellular matrix

Received: May 05, 2015     Accepted: September 11, 2015     Published: September 23, 2015

ABSTRACT

p62/IMP2 is an oncofetal protein that is overexpressed in several types of cancer, and is a member of the family of insulin-like growth factor 2 mRNA binding proteins. We previously reported that high levels of p62/IMP2 autoantibody are present in sera from cancer patients, compared to healthy individuals. Here, we report the overexpression of p62/IMP2 in tumor tissues of 72 out of 104 cases of human breast cancer, and high levels of p62/IMP2 autoantibody in patients’ sera (in 63 out of 216 cases). To explore the role of p62/IMP2 in breast cancer progression, we generated p62/IMP2 transfected variants of two human breast cancer cell lines: MDA-MB-231 and LM2-4. Using in vitro assays we found that overexpression of p62/IMP2 can increase cell migration, and reduce cell adhesion to extracellular matrix (ECM) proteins. A Human Extracellular Matrix and Adhesion Molecules qPCR array was performed with our generated variants, and it identified a group of mRNAs whose expression was altered with p62/IMP2 overexpression, including connective tissue growth factor (CTGF) mRNA – which we show to be a p62/IMP2 binding partner. Overall, our results provide new insights into the molecular mechanism by which p62/IMP2 can contribute to breast cancer progression.


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