Limits...
Inhibition of transforming growth factor beta/SMAD signal by MiR-155 is involved in arsenic trioxide-induced anti-angiogenesis in prostate cancer.

Ji H, Li Y, Jiang F, Wang X, Zhang J, Shen J, Yang X - Cancer Sci. (2014)

Bottom Line: Furthermore, As2 O3 improved the expression of miR-155 via DNA-demethylation.MiR-155, which targeted the SMAD2-3'UTR, decreased the expression and function of SMAD2.Knockdown of miR-155 abolished the As2 O3 -induced inhibitions of the TGF-β/SMAD2 signaling, the vascular endothelial growth factor secretion and angiogenesis.

View Article: PubMed Central - PubMed

Affiliation: Affiliated Nanjing Maternity and Child Health Care Hospital, Nanjing Medical University, Nanjing, China.

Show MeSH

Related in: MedlinePlus

Inhibition of transforming growth factor beta (TGF-β)/SMAD signal by demethylation-activated miR-155 is involved in arsenic trioxide-induced anti-angiogenesis in prostate cancer. VEGF, vascular endothelial growth factor.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC4317958&req=5

fig07: Inhibition of transforming growth factor beta (TGF-β)/SMAD signal by demethylation-activated miR-155 is involved in arsenic trioxide-induced anti-angiogenesis in prostate cancer. VEGF, vascular endothelial growth factor.

Mentions: Collectively, in human prostate cancer cells, As2O3 blocked angiogenesis through the inhibition of TGF-β/SMAD signal pathway in vitro and in vivo. Indeed, As2O3 improved the expression of miR-155 via DNA-demethylation. As an upstream regulator of TGF-β signaling, miR-155 decreased the expression and function of SMAD2 by targeting the SMAD2-3′UTR. Knockdown of miR-155 abolished the As2O3-induced inhibitions of TGF-β/SMAD2 signaling, VEGF secretion and angiogenesis (Fig. 7).


Inhibition of transforming growth factor beta/SMAD signal by MiR-155 is involved in arsenic trioxide-induced anti-angiogenesis in prostate cancer.

Ji H, Li Y, Jiang F, Wang X, Zhang J, Shen J, Yang X - Cancer Sci. (2014)

Inhibition of transforming growth factor beta (TGF-β)/SMAD signal by demethylation-activated miR-155 is involved in arsenic trioxide-induced anti-angiogenesis in prostate cancer. VEGF, vascular endothelial growth factor.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4317958&req=5

fig07: Inhibition of transforming growth factor beta (TGF-β)/SMAD signal by demethylation-activated miR-155 is involved in arsenic trioxide-induced anti-angiogenesis in prostate cancer. VEGF, vascular endothelial growth factor.
Mentions: Collectively, in human prostate cancer cells, As2O3 blocked angiogenesis through the inhibition of TGF-β/SMAD signal pathway in vitro and in vivo. Indeed, As2O3 improved the expression of miR-155 via DNA-demethylation. As an upstream regulator of TGF-β signaling, miR-155 decreased the expression and function of SMAD2 by targeting the SMAD2-3′UTR. Knockdown of miR-155 abolished the As2O3-induced inhibitions of TGF-β/SMAD2 signaling, VEGF secretion and angiogenesis (Fig. 7).

Bottom Line: Furthermore, As2 O3 improved the expression of miR-155 via DNA-demethylation.MiR-155, which targeted the SMAD2-3'UTR, decreased the expression and function of SMAD2.Knockdown of miR-155 abolished the As2 O3 -induced inhibitions of the TGF-β/SMAD2 signaling, the vascular endothelial growth factor secretion and angiogenesis.

View Article: PubMed Central - PubMed

Affiliation: Affiliated Nanjing Maternity and Child Health Care Hospital, Nanjing Medical University, Nanjing, China.

Show MeSH
Related in: MedlinePlus