The correlation of the nuclear localization and invasion suppression function of Syk(L) indicated that nuclear Syk possesses biological activities associated with tumor suppression in mammary epithelial cells.
Loss of SYK expression in breast tumors as a result of DNA hypermethylation promotes tumor cell proliferation and invasion and predicts shorter survival of breast cancer patients.
We analyzed the significance of epigenetic inactivation of Syk and found that reintroduction of Syk in melanoma cells dramatically reduces clonogenic survival and three-dimensional tumor spheroid growth and invasion.
Accordingly, we found that the induction of SYK expression increased the adhesion of cells to fibronectin and decreased cell migration and invasion, and that cessation of SYK overexpression increased cell migration and invasion.
By using specific antibodies and pharmacological inhibitors, we further demonstrated the involvement of Src-family tyrosine kinases, spleen tyrosine kinase, Vav, Rho, and Rho-associated kinase in Mce3C-mediated mycobacterial invasion.
CSE‑mediated focal adhesion kinase (FAK) activation resulted in the phosphorylation and activation of spleen associated tyrosine kinase (Syk)/Src proto‑oncogene, non‑receptor tyrosine kinase (Src), leading to migration and invasion of RPE cells.
Enhancing SYK activity by inducing expression of a constitutively active SYK mutant, SYK<sup>130E</sup>, increased growth factor-stimulated migration and invasion of ovarian cancer cells, which was abrogated by cortactin knockdown.