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Role for FAK in proliferation, migration, and metastasis of EL4 lymphoma cells
Author(s) -
Zhang Zhihong,
Meier Kathryn E
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.1013.6
Subject(s) - focal adhesion , cancer research , gene knockdown , biology , microbiology and biotechnology , tyrosine kinase , cell culture , signal transduction , cell migration , cell growth , mapk/erk pathway , ptk2 , tyrosine phosphorylation , kinase , protein kinase a , mitogen activated protein kinase kinase , genetics
Focal adhesion kinase (FAK) is a cytosolic protein tyrosine kinase that participates in adhesion‐mediated signaling. Our group previously established a panel of clonal cell lines derived from the EL4 mouse lymphoma line. These cell lines have been grouped into three phenotypes, only one of which forms aggressive tumors in an experimental metastasis model in syngenic mice. Numerous differences in mRNA and protein expression have been profiled between metastatic and non‐metastatic EL4 cells. One of the hallmarks of the metastatic phenotype in EL4 cells is expression of FAK. Therefore, current study examined the role of FAK in metastatic EL4 cells, using a siRNA knockdown approach. Incubation with siRNA against FAK was successful in reducing FAK protein levels in a metastatic EL4 cell line, as detected by immunoblotting. FAK knockdown significantly reduced cell proliferation in response to serum. In addition, cells with reduced FAK levels showed significantly reduced migration in response to EGF in a Boyden chamber assay. Treatment of metastatic EL4 cells with EGF enhanced FAK phosphorylation (Y397), as well as proliferation and migration. FAK knockdown blocked EGF‐induced activation of Erk. In summary, the results suggest that expression of FAK is critical for proliferation and migration of metastatic EL4 cells, and that FAK plays an important role in EGF response. Supported by NIH CA0944144.