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Syndecan-2 and KRas cooperate to induce an invasive phenotype in pancreatic cancer cells. (a) In normal cells, RACK1 binding to syndecan-2 prevents Src activation and free p120-GAP inhibits Ras signaling triggered by TKRs (b) In pancreatic ductal adenocarcinoma (PDAC) cells, p120-GAP binding to syndecan-2 activates Src and free RACK1 enhances TKR-mediated Ras activation, promoting cell proliferation, spreading, and invasion.
