Abstract

Breast cancer is the most common invasive neoplasia, and the second leading cause of death associated with cancer in women worldwide. Mammary tumorigenesis is severely linked to obesity, the potential connection is leptin. Leptin is a hormone secreted by adipocytes, which contributes to the progression of breast cancer. Cell migration, metalloproteases secretion, and invasion are cellular processes associated with various stages of metastasis. These processes are regulated by the kinases FAK and Src. In this study, we utilized the breast cancer cell lines MCF7 and MDA-MB-231 to determine the effect of leptin on FAK and Src kinases activation, cell migration, metalloproteases secretion, and invasion. By Western blot we found that leptin activates FAK and Src, and induces the localization of FAK to the focal adhesions. Specific inhibitors of FAK and Src showed that the effect exerted by leptin in cell migration, and invasion in breast cancer cells is dependent on these kinases. Moreover, by gelatin zymmography we established that leptin promotes the secretion of the extracellular matrix remodelers, MMP-2 and MMP-9, in a FAK and Src dependent manner. Our findings strongly suggest that leptin promotes the development of a more aggressive invasive phenotype in mammary cancer cells.

Details

Title
Leptin induces cell migration and invasion in a FAK-Src- dependent manner in breast cancer cells
Author
Juarez-Cruz, Juan C; Zuniga-Eulogio, Miriam Daniela; Monserrat Olea Flores; Castaneda-Saucedo, Eduardo; Mendoza-Catalan, Miguel Angel; Ortuno-Pineda, Carlos; Moreno-Godinez, Maria Elena; Villegas-Comonfort, Socrates; Padilla-Benavides, Teresita; Napoleon Navarro Tito
University/institution
Cold Spring Harbor Laboratory Press
Section
New Results
Publication year
2019
Publication date
May 8, 2019
Publisher
Cold Spring Harbor Laboratory Press
ISSN
2692-8205
Source type
Working Paper
Language of publication
English
ProQuest document ID
2221559006
Copyright
© 2019. This article is published under http://creativecommons.org/licenses/by/4.0/ (“the License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.