We have located links that may give you full text access.
Long non-coding RNA SNHG5 sponges miR-26a to promote the tumorigenesis of osteosarcoma by targeting ROCK1.
Biomedicine & Pharmacotherapy 2018 November
BACKGROUND: Osteosarcoma (OS) is one of the most common invasive malignancies of the bone. The long non-coding RNA (lncRNA) SNHG5 (small nucleolar RNA host gene 5) has been consistently shown to be involved in many cancers, although its precise function in osteosarcoma remains poorly understood. In this study, we investigated the role of SNHG5 in OS progression and the underlying mechanism.
METHODS: SNHG5 expression in 32 OS tissues and 4 OS cell lines was measured by quantitative real-time PCR (qRT-PCR). Migration, invasion, proliferation and cell cycle profiles were analyzed by established assays to determine the biological functions of SNHG5 and miR-26a in OS cells. The binding sites of miR-26a in SNHG5 and ROCK1 were predicted by the RNAhybrid 2.2 program. Luciferase reporter assay was then used to validate the direct targeting of SNHG5 with miR-26a and of Rho-associated coiled coil-containing protein kinase 1 (ROCK1) with miR-26a. The effect of SNHG5 on the ROCK signaling pathway was assessed by western blotting.
RESULTS: Elevated expression of SNHG5 was correlated with poor clinical outcome and prognosis in OS patients. SNHG5 functioned as a sponge for miR-26a and promoted proliferation, invasion and migration, and accelerated G1 to S phase transition in OS cells. SNHG5 functioned as a competing endogenous RNA (ceRNA) for miR-26a and activated the ROCK signaling pathway through the miR-26a-ROCK1 axis.
CONCLUSION: SNHG5 acts as an oncogene in OS via the SNHG5-miR-26a-ROCK1 axis and is therefore a potential novel therapeutic target for OS treatment.
METHODS: SNHG5 expression in 32 OS tissues and 4 OS cell lines was measured by quantitative real-time PCR (qRT-PCR). Migration, invasion, proliferation and cell cycle profiles were analyzed by established assays to determine the biological functions of SNHG5 and miR-26a in OS cells. The binding sites of miR-26a in SNHG5 and ROCK1 were predicted by the RNAhybrid 2.2 program. Luciferase reporter assay was then used to validate the direct targeting of SNHG5 with miR-26a and of Rho-associated coiled coil-containing protein kinase 1 (ROCK1) with miR-26a. The effect of SNHG5 on the ROCK signaling pathway was assessed by western blotting.
RESULTS: Elevated expression of SNHG5 was correlated with poor clinical outcome and prognosis in OS patients. SNHG5 functioned as a sponge for miR-26a and promoted proliferation, invasion and migration, and accelerated G1 to S phase transition in OS cells. SNHG5 functioned as a competing endogenous RNA (ceRNA) for miR-26a and activated the ROCK signaling pathway through the miR-26a-ROCK1 axis.
CONCLUSION: SNHG5 acts as an oncogene in OS via the SNHG5-miR-26a-ROCK1 axis and is therefore a potential novel therapeutic target for OS treatment.
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