SFK expression, as measured by immunoblotting with an antibody sp

SFK expression, as measured by immunoblotting with an antibody specifically recognizing Src, Fyn, and Yes, were elevated in 25 of 52 breast tumors. c-Src kinase and STAT3 activated hepatocyte growth factor expression in breast carcinoma cells [7, 8]. Enhanced c-Src activity is also one potential mechanism leading to tamoxifen-resistant growth in breast cancer, and activation of c-Src and Fak has a close relationship with distant recurrence in hormone-treated, ER-positive breast cancer [9]. In recent studies, elevated c-Src activity was directly involved

in the disruption of cell-cell adhesions in tamoxifen-resistant breast cancer cell lines, indicating that activated c-Src plays a role in the mislocalization of adhesion proteins [10]. Therefore, c-Src and c-Yes play important roles in colon cancer and breast cancer. However, a very small Caspase inhibitor number of studies have been conducted on SFK expression in skin cancer, and there is some controversy as to whether c-Src or c-Yes affects melanoma. By measuring tyrosine-specific HDAC activity assay kinase activity for c-Src expression in human beta-catenin phosphorylation melanoma tissues kinase activity in melanoma was found to be greater than that in normal skin regardless of the type of melanoma or the metastatic

site [11]. In one study, Src kinase inhibitor dasatinib inhibited melanoma cell migration and invasion by inducing cell cycle arrest and apoptosis [12]. STAT3, which has been shown to play an important role in tumor cell proliferation and survival,

and c-Src tyrosine kinase are activated in melanoma cell lines. Melanoma cells undergo apoptosis when either Src kinase activity or STAT3 signaling is inhibited [13]. This supports the fact that Src activated STAT3 signaling has a key role in the survival and growth of melanoma tumor cells. c-Src activation also affects epidermal growth factor of STAT in head and neck SCCs and promotes the invasion and progression of SCC [14–16]. On the contrary, it has been reported that c-Yes expression and kinase activity in human melanoma cell lines are greater than that in normal melanocyte cell lines, and that c-Src expression and activity are not different in human melanoma cell lines compared to normal melanocyte cell lines [17]. Similarly, it was demonstrated in another study that c-Yes tyrosine kinase Phosphoglycerate kinase was activated more in human brain-metastatic melanoma cell lines by stimulation of neurotropin and nerve growth factor, whereas c-Src was not affected [18]. These results show that c-Yes is more important than c-Src in melanoma progression and metastasis. Therefore, we studied the expression of both c-Src and c-Yes in overall human skin cancer tissues including MM, SCC, and BCC using western blotting and immunochemistry. Our study results show that c-Src was expressed in all skin cancer tissues, but not in normal skin tissues. c-Yes was expressed in MM and SCC, but not in normal skin tissues or BCC.

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