Journal Article
Research Support, Non-U.S. Gov't
Add like
Add dislike
Add to saved papers

miR-96 promotes cell proliferation and clonogenicity by down-regulating of FOXO1 in prostate cancer cells.

Medical Oncology 2014 April
The present study aimed to investigate the biological functions of miR-96 in the processes of proliferation and clonogenicity in the prostate cancer cells. miR-96 was identified to be markedly up-regulated in prostate cancer cell and cancer tissues compared with normal prostate cell and normal prostate tissues by microarray method and RT-PCR analysis. Down-regulation of miR-96 expression reduced the proliferation and colony formation ability of PC3 prostate cancer cells, while over-expression of miR-96 induced proliferation and colony formation ability of LNCaP prostate cancer cells. Forkhead box protein O1 (FOXO1) is key tumor suppressors and has been shown to play key roles in the regulation of diverse cellular processes, including cell proliferation, differentiation, cell cycle progression and apoptosis. The expression level of FOXO1 was strikingly up-regulated in PC3 cells after transfected with miR-96 inhibitor, and FOXO1 expression was down-regulated in LNCaP cells after transfected with miR-96 mimics. miR-96 may play a vital role in promoting cell proliferation in human prostate cancer cells. Inhibition of miR-96 caused expression increase of tumor suppressor gene FOXO1, thus manipulating miR-96 expression may be a promising approach in treatment of prostate cancer.

Full text links

We have located links that may give you full text access.
Can't access the paper?
Try logging in through your university/institutional subscription. For a smoother one-click institutional access experience, please use our mobile app.

Related Resources

For the best experience, use the Read mobile app

Mobile app image

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 Toggle icon

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