LncRNA H19/miR ‐194/PFTK1 axis modulates the cell proliferation and migration of pancreatic cancer

MiR ‐194 messenger RNA expression was dramatically downregulated in pancreatic ductal adenocarcinoma (PDAC) tissues, and was negatively correlated with long noncoding RNA (lncRNA) H19 and PFTK1, suggesting that rescuing miR‐194 expression in PDAC, therefore inhibiting lncRNA H19 and PFTK1, subsequen tly suppressing PDAC cell proliferation and migration might make contribution to the treatment of PDAC. AbstractPancreatic ductal adenocarcinoma (PDAC) remains a huge challenge due to its high mortality and morbidity; gene therapy might be a promising treatment for PDAC. The critical role of Wnt ‐signaling pathway in cancer pathogenesis has been widely recognized; cyclin‐dependent kinase 14 (CDK14, PFTK1)‐induced low‐density lipoprotein receptor‐related proteins 5/6 (LRP5/6) phosphorylation is an important issue in Wnt‐signaling activation. Long noncoding RNA (LncRNA)‐microRNA (miRNA)‐messenger RNA (mRNA) modulating the pathogenesis of cancers has been regarded as a major mechanism. In the current study, upregulated lncRNAs positively correlated with PFTK1 were analyzed and selected using The Cancer Genome Atlas (TCGA) database. Of them, lncRNA H19 can activate Wnt sig naling in cancers. In PDAC tissues, the expression of H19 and PFTK1 were upregulated; H19 knockdown suppressed the cell proliferation and migration of PDAC, while PFTK1 overexpression partially attenuated the suppressive effect of H19 knockdown. As analyzed by TCGA and predicted by online tools, ...
Source: Journal of Cellular Biochemistry - Category: Biochemistry Authors: Tags: RESEARCH ARTICLE Source Type: research