We have located links that may give you full text access.
The role of miR-18a in gastric cancer angiogenesis.
Hepato-gastroenterology 2013 October
BACKGROUND/AIMS: To investigate the effect of miR-18a on angiogenesis in gastric cancer.
METHODOLOGY: We generated stable cell lines overexpressing miR-18a in SGC-7901 cells. Cell proliferation was assessed by the MTT assay. The effects of miR-18a overexpression on tumor growth and angiogenesis were assessed. Because of the key role of mammalian target of rapamycin (mTOR) signaling in gastric cancer progression, we also tested whether miR-18a overexpression affected the mTOR pathway.
RESULTS: Ectopic expression of miR-18a significantly diminished cell proliferation in SGC-7901 cells (p<0.01). miR-18a overexpression significantly retarded SGC-7901 xenograft growth by 71.8% in vivo, and caused a marked reduction in tumor angiogenesis assessed by CD31-stained microvessel count. Western blot analysis of the xenografts showed that miR-18a overexpression substantially reduced the phosphorylation of two mTOR substrates, S6K1 and 4E-BPl, indicative of art inactivation of the mTOR pathway. Accompanying with the mTOR inactivation, the angiogenic factors, hypoxia-inducible factor 1 alpha and vascular endothelial growth factor, were significantly downregulated.
CONCLUSIONS: These data highlighted an important role for miR-18a in controlling gastric cancer growth and angiogenesis, therefore offering a possible therapeutic strategy against this malignancy.
METHODOLOGY: We generated stable cell lines overexpressing miR-18a in SGC-7901 cells. Cell proliferation was assessed by the MTT assay. The effects of miR-18a overexpression on tumor growth and angiogenesis were assessed. Because of the key role of mammalian target of rapamycin (mTOR) signaling in gastric cancer progression, we also tested whether miR-18a overexpression affected the mTOR pathway.
RESULTS: Ectopic expression of miR-18a significantly diminished cell proliferation in SGC-7901 cells (p<0.01). miR-18a overexpression significantly retarded SGC-7901 xenograft growth by 71.8% in vivo, and caused a marked reduction in tumor angiogenesis assessed by CD31-stained microvessel count. Western blot analysis of the xenografts showed that miR-18a overexpression substantially reduced the phosphorylation of two mTOR substrates, S6K1 and 4E-BPl, indicative of art inactivation of the mTOR pathway. Accompanying with the mTOR inactivation, the angiogenic factors, hypoxia-inducible factor 1 alpha and vascular endothelial growth factor, were significantly downregulated.
CONCLUSIONS: These data highlighted an important role for miR-18a in controlling gastric cancer growth and angiogenesis, therefore offering a possible therapeutic strategy against this malignancy.
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