Fig. 8

TFCP2 feedback induced the expression of ITGA2 as a transcription factor in pancreatic cancer cells. a GEPIA database was searched to determine the correlation between the mRNA expression of TFCP2 and ITGA2 in the PDAC samples. P-and R-values are indicated in the figure. b RT-PCR was used to determine the mRNA expression level of ITGA2 in the PANC-1 and AsPC-1 cells infected with sh-Control or sh-TFCP2s. GAPDH served as an internal reference and repeated in triplicates. ns, not significant; ***P < 0.001. c Western blot analysis was used to determine the protein expression level of ITGA2 in the PANC-1 and AsPC-1 cells infected with sh-Control or sh-TFCP2s. GAPDH served as an internal reference. d RT-PCR was used to determine the mRNA expression level of ITGA2 in the PANC-1 and AsPC-1 cells infected with pcDNA3.1 or TFCP2 plasmids. GAPDH served as an internal reference and repeated in triplicates. ns, not significant; ***P < 0.001. e Western blot analysis was used to determine the protein expression level of ITGA2 in the PANC-1 and AsPC-1 cells infected with pcDNA3.1 or TFCP2 plasmids. GAPDH served as an internal reference. f EPD database was searched to determine the potential binding sites of TFCP2 in the promoter region of ITGA2 genes. g ChIP-qPCR of TFCP2 in the PANC-1 and AsPC-1 cells. All the data are shown as the mean values ± SD from three independent replicates. ***P < 0.001. h Working model, showing that the ITGA2 inhibits the activation of TGF-β pathway in pancreatic cancer via TFCP2-SMAD2 axis, and TFCP2 feedback induced the expression of ITGA2 as a transcription factor