Abstract

ROLE OF FOCAL ADHESION KINASE INHIBITORS AS ANTICANCER AGENTS

Madhuri Haraklal Jain and Rakesh Ravindra Somani*

Abstract

Focal adhesion kinase (FAK) is a cytoplasmic protein tyrosine kinase that enables activation by integrins or growth factor receptors in different types of human cancers. It is overexpressed and activated in cancer. FAK mediates metastasis and tumour proliferation. FAK mediates metastasis and tumour proliferation. The kinase-dependent and kinase-independent role of FAK controls cell invasion, movement, gene expression, survival and self-renewal of cancer stem cell. FAK activation and overexpression are usually investigated in metastatic or primary cancers which are correlated with the poor clinical outcome. It highlights FAK as potential portent marker and anticancer target. Various FAK inhibitors target FAK-scaffolding functions and FAK kinase activity which impairs cancer development in preclinical or clinical trials. FAK inhibitors decreases metastasis and growth of tumour in many preclinical models and have shown biological activity with less number of adverse reactions. In this review, we give an overview of different FAK signaling pathways in cancer, its role in cellular function that provide rationale and support for future therapeutic approach in cancer treatment.

Keywords: Angiogenesis, Cell adhesion, Cell invasion, Cell proliferation, Cell survival, Focal adhesion kinase.