Abstract
Aim: To study Expression and Phosphorylation status of Focal Adhesion Kinase (FAK) in Human Breast Cancer tissue. To study the relation of FAK with standard clinicopathological parameters of Human Breast Cancer. Methods: Tissue collection, Protein extraction, RNA isolation, Western Blot, Immunohistochemistry, RT-PCR, ELISA, Statistical analysis. Results: All the four techniques showed upregulated expression, phosphorylation (Tyr-397) and processing of FAK in human breast cancer tissue compared to the adjacent non-tumor tissue of the same patient. Upregulation of FAK was found to be increased parallely with the advancement of cancer. Localisation of FAK was found to be membrano-cytoplasmic. FAK is upregulated both in protein and mRNA level. Expression and phosphorylation of FAK is increased specifically in the tumor regions compared to the surrounding non-tumor region. Upregulation of FAK was frequently found in ER-positive and PR-positive but Her2/neunegative breast cancer cases. Conclusion: FAK has crucial role in development and progression of human breast cancer. FAK may be considered as an indicator of human breast cancer progression. FAK processing may be considered as an indicator of invasive potential of breast cancer. FAK may be considered as a clinical indicator of human breast cancer development and progression.
Highlights
Focal adhesion kinase (FAK) is a 125 kD nonreceptor protein tyrosine kinase that localizes at the cellular adhesion points
Expression and phosphorylation of FAK is increased in the tumor regions compared to the surrounding non-tumor region
FAK may be considered as an indicator of human breast cancer progression
Summary
Focal adhesion kinase (FAK) is a 125 kD nonreceptor protein tyrosine kinase that localizes at the cellular adhesion points. It is a crucial mediator of signaling events between cells and cell surrounding extracellular matrix (ECM). Interaction of FAK with a number of signaling molecules situates it at a junction of signal transduction network and regulates cell migration [5,6,7,8,9] and apoptosis [10,11,12,13,14,15,16,17], cell proliferation [18,19,20,21,22] etc. In response to clustering of integrins due to ligand interaction, FAK is get activated by an autophosphorylation at Tyrosine-397 [23]
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