Rab11a Is Overexpressed in Gastric Cancer and Regulates FAK/AKT Signaling

Figure 7

Rab11a regulates proliferation, chemosensitivity and related proteins through FAK signaling. (a) MTT assay showed that FAK inhibitor downregulated cell viability 3 days after Rab11a transfection. FAK inhibitor also abolished the growth promoting effect of Rab11a. (b) Cell viability was examined after 2.5 μg/mL cisplatin treatment. FAK inhibitor suppressed Rab11a mediated cisplatin resistance. (c) FAK inhibitor PF-573228 was used in cells transfected with Rab11a plasmid or control vector. PF-573228 significantly decreased phosphorylation of AKT and FAK. PF-573228 also decreased cyclin D1, MMP2, and Bcl-2 protein expression. In cells treated with PF-573228, Rab11a did not increase cyclin D1, MMP2, and Bcl-2 protein. Quantification of western blot that was performed was indicated.

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