Fig. 1
Abnormal KRAS activation induced the overexpression of ITGA2 in pancreatic cancer cells. a ITGA2 is one of the KRAS up-regulated surfaceome in different pancreatic ductal adenocarcinoma (PDAC) cell lines (AK10965, AK192, AK196) [16]. b Cancer molecular expression profile data of cBioPortal, showing the expression of ITGA2 in wt-KRAS and mut-KRAS pancreatic cancer. c RT-PCR was used to determine the mRNA expression level of ITGA2 in PANC-1 and AsPC-1 cells treated with KRASG12D inhibitor (KRpep-2d, 10uM). GAPDH served as an internal reference and repeated in triplicates. ***P < 0.001. d Western blot analysis for determining the protein expression level of ITGA2 in the PANC-1 or AsPC-1 cells treated with KRASG12D inhibitor (KRpep-2d, 10uM). GAPDH served as an internal reference. e RT-PCR was used to determine the expression level of ITGA2 in PANC-1 and AsPC-1 cells treated with ERK 1/2 inhibitors (U0126, 10uM). GAPDH served as an internal reference and repeated in triplcates. ***P < 0.001. f Western blot analysis for detrmining the protein expression level of ITGA2 in the PANC-1 or AsPC-1 cells treated with ERK1/2 inhibitor (U0126, 10uM). GAPDH served as an internal reference. g RT-PCR was used to determine the expression level of ITGA2 in PANC-1 and AsPC-1 cells infected with KRASG12D plasmids. GAPDH served as an internal reference and repeated in triplcates. ***P < 0.001. h Western blot analysis for determining the protein expression level of ITGA2, ERK1/2, p-ERK1/2, KRAS in the PANC-1 or AsPC-1 cells infected with KRASG12D plasmids. GAPDH served as an internal reference