Fig. 5

PART1 functions as a ceRNA by sponging miR-122. a The putative miR-122 binding sites of the wild-type (Wt) and mutant (Mut) sequences of PART1. b qRT-PCR analysis of miR-122 expression in cancer tissues (n = 45) and para-tumor normal tissues (n =45). c The expression of miR-122 in AsPC-1 and BxPC-3 cells was increased by PART1 knockdown. d qRT-PCR confirmed miR-122 expression in AsPC-1 and BxPC-3 cell after being transfected with miR-122 inhibitor and inhibitor control. e, f The PART1-Wt or PART1-Mut reporter vector was cotransfected with miR-122 inhibitor and inhibitor control into AsPC-1 and BxPC-3 cells, and the relative luciferase activity was detected. g RIP assay with anti-Ago2 and anti-IgG antibodies was performed in AsPC-1 and BxPC-3 cells, and the coprecipitated RNA was used to quantify PART1 expression. *P < 0.05, **P < 0.01, and ***P < 0.001