Like silenced c-met and ron will lead to inhibition of cell migration and invasion by p42/44mapk phosphorylation and reduce stat 3 activation in cancer cell line. With this pathway, can I apply it in diabetic cell line if I spot there is reduced activation of stat 3 and mapk then link it to less expression of ron?
Can I use it to explain the reduction of wound closure on cell proliferation and cell migration based on an assumption basis or as an indicator of what can that pathway leads to? Or even, what can the receptor do relate to cell migration?
Their are many proteins that are upregulated or downregulated in normal cells compared to cancer cells, few eg are p53, p21, CDKs, cyclins, Stat 1,3, EGFR, ERK1/2 etc.
I am only interested on the tyrosine kinase receptors and their interactions in cell migration/ cell proliferation. So I wished to use proven mechanism to understand what is the role of that certain tyrosine kinase receptor can do in a rough manner on normal/diabetic cell line.
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