High expression of FBP17 in invasive breast cancer cells promotes invadopodia formation
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Metastatic spread of the cancer is usually the consequence of the activation of signaling pathways that generate cell motility and tissue invasion. Metastasis involves the reorganization of cytoskeleton and cell shape for the swift movement of the cells through extracellular matrix. Previously, we have described the invasive and metastatic role played by one of the members (Toca-1) of CIP4 subfamily of F-BAR proteins. In the present study, we address the role of another member (FBP17) of same family in the invasion breast cancer cells. Here, we report that the formin-binding protein 17 (FBP17) is highly expressed at both mRNA and protein levels in breast cancer cells. The study showed the association of FBP17 with cytoskeletal actin regulatory proteins like dynamin and cortactin. To determine its role in extracellular matrix (ECM) degradation, we achieved stable knockdown of FBP17 in MDA-MB-231 cells. FBP17 knockdown cells showed a defect and were found to be compromised in the degradation of ECM indicating the role of FBP17 in the invasion of breast cancer cells. Our results suggest that FBP17 is highly expressed in breast cancer cells and facilitates the invasion of breast cancer cells.
KeywordsFormin-binding protein 17 Breast cancer Invadopodia Extracellular matrix
We acknowledge Department of Science and Technology-Science and Engineering Research Board (DST_SERB), EMR/2015/000761, Government of India for extramural research funding to Harish Chander and Central University of Punjab for additional support. We thank Andrew Craig, Queen’s University, Kingston, Canada for Cell Lines and additional support.
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Conflict of interest
The authors declare no conflict of interest.
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