Fig. 5

Alterations in the H19/miR-29c-5p/ATF2/ECM1 Axis during Pancreatic Cancer Progression. (A) The differential mRNA expression of ATF2 and ECM1 in pancreatic cancer in the TCGA database; in pathological immunohistochemistry, the protein expression of ATF2 and ECM1 was significantly increased in the cancer nests of clinical patients compared to the adjacent tissues, *p < 0.05, **p < 0.01, ***p < 0.001.). (B) The predicted binding sites of miR-29c-5p on the 3’UTR of ATF2 and the sequence illustration of the ATF2 binding site of the transcription factor. (C) In the TCGA database, miR-29c was negatively correlated with the expressions of ATF2 and ECM1. (D) Western blot verification of the protein levels of ATF2 and ECM1; knockdown of H19 decreased ATF2 and ECM1, while miR-29c-5p mimics exhibited a similar inhibitory effect. β-actin was utilized as a loading control, *p < 0.05, **p < 0.01, ***p < 0.001.)