We have located links that may give you full text access.
High expression of microRNA-4295 contributes to cell proliferation and invasion of pancreatic ductal adenocarcinoma by the down-regulation of Glypican-5.
Biochemical and Biophysical Research Communications 2018 Februrary 27
A growing amount of evidence has documented that Glypican-5 (GPC5) is an important regulator of tumor progression. However, little is known about the role of GPC5 in pancreatic ductal adenocarcinoma (PDAC). In this study, we aimed to investigate the potential function and regulatory mechanism of GPC5 in PDAC. We found that GPC5 expression was significantly down-regulated in PDAC cell lines. The overexpression of GPC5 inhibited cell proliferation and the invasion of PDAC cells. In addition, the overexpression of GPC5 suppressed Wnt/β-catenin signaling in PDAC cells. Bioinformatic analysis predicted that GPC5 was a target gene of microRNA-4295 (miR-4295). The inhibition of miR-4295 significantly up-regulated the expression of GPC5. Moreover, the inhibition of miR-4295 inhibited the proliferation, invasion and Wnt/β-catenin signaling in PDAC cells. Notably, the knockdown of GPC5 partially reversed the anti-tumor effect of miR-4295 inhibition. Taken together, our results suggest GPC5 as a tumor suppressor in PDAC and its expression is possibly regulated by miR-4295. Our study indicates that the miR-4295/GPC5 axis may play an important role in the pathogenesis of PADC and has potential applications for the development of PDAC therapy.
Full text links
Related Resources
Get seemless 1-tap access through your institution/university
For the best experience, use the Read mobile app
All material on this website is protected by copyright, Copyright © 1994-2024 by WebMD LLC.
This website also contains material copyrighted by 3rd parties.
By using this service, you agree to our terms of use and privacy policy.
Your Privacy Choices
You can now claim free CME credits for this literature searchClaim now
Get seemless 1-tap access through your institution/university
For the best experience, use the Read mobile app