H19 enhances pancreatic cancer proliferation and invasion by reducing miR-29c-5p's inhibitory effects on ATF2/ECM1.

Pancreatic ductal adenocarcinoma is a lethal malignancy with few therapeutic options. Identifying novel molecular targets is essential for treating this illness. This work suggests that the long non-coding RNA H19 exhibits a carcinogenic role in pancreatic ductal adenocarcinoma (PDAC). Analysis of TCGA data and clinical samples revealed a significant elevation of H19 in PDAC tissues. This elevation was associated with a poor outcome and a heightened likelihood of metastatic spread. In this study, H19 was demonstrated to enhance the proliferation, migration, and invasion of PDAC cells via the ceRNA pathway. This was achieved by sponging miR-29c-5p and reducing its regulation of ATF2, hence enhancing the expression of ECM1. Functional investigations indicated that H19 was accountable for generating these effects. The outcomes of rescue experiments indicated that the suppression of ATF2 and ECM1 by miR-29c-5p was effectively counteracted with the overexpression of H19. In vivo experiments revealed that the inhibition of H19 resulted in decreased levels of ATF2 and ECM1, together with a diminished tumor development in xenograft mice. An elevated expression of ATF2 and ECM1 was associated with advanced stages of pancreatic cancer and reduced survival rates in clinical contexts. Our findings implicate the H19/miR-29c-5p/ATF2/ECM1 axis as a potential therapeutic target in pancreatic ductal adenocarcinoma progression.