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Studies on Focal Adhesion Kinase in human breast cancer cell MDA-MB-231

Author(s): Jaydip Biswas | Amitava Chatterjee | Sekhar Pal | Kirat Kumar Ganguly | Triparna Sen

Journal: Journal of Biophysical Chemistry
ISSN 2153-036X

Volume: 02;
Issue: 01;
Start page: 29;
Date: 2012;
Original page

Keywords: FAK | Fibronectin | MMP-9 | Cell Migration | Breast Cancer

AIM: 1) To study the participation of Focal Adhesion Kinase (FAK) in regulation of Breast Cancer cell mi- gration in relation with MMP-9 and other signaling proteins. 2) To study the effect of some natural prod- ucts on FAK. METHODS: Cell culture, Western Blot, Immunoprecipitation, Immunocytochemistry, Zymogra- phy, SiRNA transfection, RT-PCR, Real-Time PCR. RESULTS: For our study on FAK, we selected invasive Breast Cancer cell line MDA-MB-231 and trea- ted the cells with Fibronectin (FN). Treatment of FN was found to increase FAK expression, phosphorylation (Tyr 397). FAK was found to be involved in re- gulation of breast cancer cell migration and MMP-9 expression, activity. Fi-bronectin increases association of FAK with integrin α5β1, Paxillin, Actin, ERK, PI3K and localization at Focal Adhesion sites. FAK was found to be involved in modulation of ERK and PI3K phosphorylation. Moreover, FAK signal was found to be transduced through ERK and PI3K, which modulate MMP-9 and thereby cell migration. CONCLUSION: FAK expres-sion, phosphorylation and pro- cessing are induced in response to Cell-ECM interactions. Integrin α5β1 is involved in FN induced FAK phosphorylation. FAK is a potent regulator of MMP-9 expression and activity. FAK is involved in regulation of ERK and PI3K phosphorylation. ERK and PI3K are involved in FAK regulated MMP-9 expression & activity. FAK regulates MMP-9 expression and activity and thereby migration of human breast cancer cell. By the regulation of FAK, cell attachment and migration may be regulated by Curcumin, ATRA or EGCG treatment. It may be concluded that invasive potential of breast cancer cells may be modulated by regulation of FAK.
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