Abstract

Abstract Background: Focal adhesion kinase is a tyrosine kinase that plays a critical role at focal adhesion sites in cell mobility and migration. The over-expression and mutation of FAK, which promotes tumor cell invasion and survival, frequently occurs in tumors, allowing FAK to be recognized as a cancer-relevant gene and a potential target for cancer treatment. The vast majority of evidence has revealed that the deregulation of alternative splicing processes often occurs in cancer-associated genes and leads to tumorigenesis. Results: From 102 breast cancer tissue samples, we found six samples contained the 26 exon deletion FAK associated with a mutation at the 3192 bp site(CDS), but this 26 exon deletion FAK was not observed in the samples derived from 101 normal tissues. Interestingly, the 26 exon deletion FAK, which possesses the same kinase activity and biological function as wild-type FAK, is resistant to caspase-mediated cleavage and prevents breast cancer cells from apoptosis, promoting breast cancer cells survival. Conclusion: Therefore, our study revealed that the aberrant splicing of the FAK gene may promote tumorigenesis, providing a new method for diagnosing breast cancer and a potentially important target for breast cancer treatment. Citation Information: Cancer Res 2013;73(24 Suppl): Abstract nr P5-07-09.

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