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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: Briefly, As2 O3 inhibited the activations/expressions of both TGFβ-induced and endogenous SMAD2/3.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.

View Article: PubMed Central - PubMed

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

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As2O3 attenuates the angiogenic abilities in prostate carcinoma cells. (a and b) PC-3 and LNCaP cells were treated by 0, 0.5, 1, 2, or 4 μM As2O3 for 48 h, respectively, and the mediums were collected for further investigation. (a) The cell viabilities were evaluated in triplicate by WST-8 hydrolysis using a Cell Counting Kit-8 assay. (b) The vascular endothelial growth factor (VEGF) secreted by PC-3 and/or LNCaP cells in the mediums were determined in triplicate by ELISA. *P < 0.05 and **P < 0.01 compared with medium control cells.(c and d) After PC-3 (c) or LNCaP (d) cells were pre-treated by 0 or 2 μM As2O3 for 48 h, followed by a conventional culture in fresh medium for another 24 h, the mediums were collected. Human umbilical vein endothelial cells (HUVEC) were exposed to such mediums as indicated for 6 h, respectively, and the formations of tube were evaluated as described in the section “Materials and Methods”. Bars = 250 μm.
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fig01: As2O3 attenuates the angiogenic abilities in prostate carcinoma cells. (a and b) PC-3 and LNCaP cells were treated by 0, 0.5, 1, 2, or 4 μM As2O3 for 48 h, respectively, and the mediums were collected for further investigation. (a) The cell viabilities were evaluated in triplicate by WST-8 hydrolysis using a Cell Counting Kit-8 assay. (b) The vascular endothelial growth factor (VEGF) secreted by PC-3 and/or LNCaP cells in the mediums were determined in triplicate by ELISA. *P < 0.05 and **P < 0.01 compared with medium control cells.(c and d) After PC-3 (c) or LNCaP (d) cells were pre-treated by 0 or 2 μM As2O3 for 48 h, followed by a conventional culture in fresh medium for another 24 h, the mediums were collected. Human umbilical vein endothelial cells (HUVEC) were exposed to such mediums as indicated for 6 h, respectively, and the formations of tube were evaluated as described in the section “Materials and Methods”. Bars = 250 μm.

Mentions: First, we determined the effects of As2O3 on the viabilities of human prostate carcinoma PC-3 and LNCaP cells. As shown in Figure 1(a), there were decreases of viabilities in cells exposed to 4 μM As2O3; however, no detectable attenuations of viabilities were observed in cells exposed to 0.5, 1 and 2 μM As2O3. Next, we used ELISA to investigate the effects of As2O3 on the VEGF secretion in these cells. As shown in Figure 1(b), As2O3 inhibited the secretions of VEGF in a dose-dependent manner. Finally, we used the tube formation assay to further detect the functions of As2O3 in the angiogenic ability of prostate carcinoma cells. To avoid the addition of As2O3 to the endothelial cells in the tube formation assay, we pre-treated PC-3 and/or LNCaP cells with 0 or 2 μM As2O3 for 48 h, followed by a conventional culture in fresh medium for another 24 h. The conditioned mediums were then collected. We treated human umbilical vein endothelial cells (HUVEC) with these conditioned mediums, respectively. Our data showed that there was decreased cell viability (Fig. S1a) and attenuated formations of tubes in HUVEC (Fig. 1c,d) incubated with the conditioned mediums collected from As2O3-pre-treated cells. Importantly, there was no detectable inhibition of tube formation after HUVEC were directly exposed to As2O3 (Fig. S1b). These results suggest that As2O3 attenuates the angiogenic abilities of prostate carcinoma cells, in which the inhibitions of VEGF secretion are involved.


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)

As2O3 attenuates the angiogenic abilities in prostate carcinoma cells. (a and b) PC-3 and LNCaP cells were treated by 0, 0.5, 1, 2, or 4 μM As2O3 for 48 h, respectively, and the mediums were collected for further investigation. (a) The cell viabilities were evaluated in triplicate by WST-8 hydrolysis using a Cell Counting Kit-8 assay. (b) The vascular endothelial growth factor (VEGF) secreted by PC-3 and/or LNCaP cells in the mediums were determined in triplicate by ELISA. *P < 0.05 and **P < 0.01 compared with medium control cells.(c and d) After PC-3 (c) or LNCaP (d) cells were pre-treated by 0 or 2 μM As2O3 for 48 h, followed by a conventional culture in fresh medium for another 24 h, the mediums were collected. Human umbilical vein endothelial cells (HUVEC) were exposed to such mediums as indicated for 6 h, respectively, and the formations of tube were evaluated as described in the section “Materials and Methods”. Bars = 250 μm.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

fig01: As2O3 attenuates the angiogenic abilities in prostate carcinoma cells. (a and b) PC-3 and LNCaP cells were treated by 0, 0.5, 1, 2, or 4 μM As2O3 for 48 h, respectively, and the mediums were collected for further investigation. (a) The cell viabilities were evaluated in triplicate by WST-8 hydrolysis using a Cell Counting Kit-8 assay. (b) The vascular endothelial growth factor (VEGF) secreted by PC-3 and/or LNCaP cells in the mediums were determined in triplicate by ELISA. *P < 0.05 and **P < 0.01 compared with medium control cells.(c and d) After PC-3 (c) or LNCaP (d) cells were pre-treated by 0 or 2 μM As2O3 for 48 h, followed by a conventional culture in fresh medium for another 24 h, the mediums were collected. Human umbilical vein endothelial cells (HUVEC) were exposed to such mediums as indicated for 6 h, respectively, and the formations of tube were evaluated as described in the section “Materials and Methods”. Bars = 250 μm.
Mentions: First, we determined the effects of As2O3 on the viabilities of human prostate carcinoma PC-3 and LNCaP cells. As shown in Figure 1(a), there were decreases of viabilities in cells exposed to 4 μM As2O3; however, no detectable attenuations of viabilities were observed in cells exposed to 0.5, 1 and 2 μM As2O3. Next, we used ELISA to investigate the effects of As2O3 on the VEGF secretion in these cells. As shown in Figure 1(b), As2O3 inhibited the secretions of VEGF in a dose-dependent manner. Finally, we used the tube formation assay to further detect the functions of As2O3 in the angiogenic ability of prostate carcinoma cells. To avoid the addition of As2O3 to the endothelial cells in the tube formation assay, we pre-treated PC-3 and/or LNCaP cells with 0 or 2 μM As2O3 for 48 h, followed by a conventional culture in fresh medium for another 24 h. The conditioned mediums were then collected. We treated human umbilical vein endothelial cells (HUVEC) with these conditioned mediums, respectively. Our data showed that there was decreased cell viability (Fig. S1a) and attenuated formations of tubes in HUVEC (Fig. 1c,d) incubated with the conditioned mediums collected from As2O3-pre-treated cells. Importantly, there was no detectable inhibition of tube formation after HUVEC were directly exposed to As2O3 (Fig. S1b). These results suggest that As2O3 attenuates the angiogenic abilities of prostate carcinoma cells, in which the inhibitions of VEGF secretion are involved.

Bottom Line: Briefly, As2 O3 inhibited the activations/expressions of both TGFβ-induced and endogenous SMAD2/3.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.

View Article: PubMed Central - PubMed

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

Show MeSH
Related in: MedlinePlus