Limits...
Down-regulation of mir-221 and mir-222 restrain prostate cancer cell proliferation and migration that is partly mediated by activation of SIRT1.

Yang X, Yang Y, Gan R, Zhao L, Li W, Zhou H, Wang X, Lu J, Meng QH - PLoS ONE (2014)

Bottom Line: MiR-221 and miR-222 were highly expressed in PC-3 cells compared with in LNCap cells.Cells transfected with siSIRT1 showed increased migration and a decreased apoptosis rate, but there was no significant effect on cell proliferation compared with the controls.These effects are potentially mediated by up-regulation of SIRT1.

View Article: PubMed Central - PubMed

Affiliation: Wenzhou Medical University School of Laboratory Medicine and Life Sciences, Wenzhou, Zhejiang, China.

ABSTRACT
Studies have shown that miR-221 and miR-222 are deregulated in many cancers, including prostate cancer. Nevertheless, the biological role and the underlying mechanisms of miR-221 and miR-222 in the pathogenesis of androgen-independent prostate cancer are still not clear. The proliferation, apoptosis, cell cycle distinction, and migration capacity of prostate cells were determined following transfection of miR-221 or miR-222 inhibitor. The biological impact and regulation of SIRT1 on prostate cancer cells were investigated. MiR-221 and miR-222 were highly expressed in PC-3 cells compared with in LNCap cells. After miR-221 or miR-222 expression was inhibited, the proliferation and migration rates of PC-3 cells decreased and the apoptosis rate increased. Moreover, SIRT1 protein was up-regulated in cells after they were transfected with miR-221 or miR-222 inhibitor. Cells transfected with siSIRT1 showed increased migration and a decreased apoptosis rate, but there was no significant effect on cell proliferation compared with the controls. There was a negative correlation between miR-221 or miR-222 and SIRT1, but no direct target relationship was identified. These data demonstrate that miR-221 and miR-222 are highly expressed in PC-3 cells. Their inhibition leads to reduced cell proliferation and migration and increased apoptosis in prostate cancer cells. These effects are potentially mediated by up-regulation of SIRT1.

Show MeSH

Related in: MedlinePlus

Effects of miR-221 inhibitor and miR-222 inhibitor on PC-3 cell migration.(A) Wound healing assay shows the closure rates of cells transfected with pEX-5 (empty vector plasmid), miR-221 inhibitor, or miR-222 inhibitor. (B) Quantitation of wound closure rates at different time points. (C) Transwell assay shows that the cells penetrated the insert membrane. (D) Quantitation of the number of cells that penetrated the insert membrane. Data represent the mean value ± SEM from three separate experiments. *,# P<0.05 vs pEX-5, **,## P<0.01 vs pEX-55).
© Copyright Policy
Related In: Results  -  Collection


getmorefigures.php?uid=PMC4043919&req=5

pone.0098833-g005: Effects of miR-221 inhibitor and miR-222 inhibitor on PC-3 cell migration.(A) Wound healing assay shows the closure rates of cells transfected with pEX-5 (empty vector plasmid), miR-221 inhibitor, or miR-222 inhibitor. (B) Quantitation of wound closure rates at different time points. (C) Transwell assay shows that the cells penetrated the insert membrane. (D) Quantitation of the number of cells that penetrated the insert membrane. Data represent the mean value ± SEM from three separate experiments. *,# P<0.05 vs pEX-5, **,## P<0.01 vs pEX-55).

Mentions: As shown in Figures 5A and B, the closure rates of the miR-221 inhibitor and miR-222 inhibitor groups were lower than was that of pEX-5 group. For instance, the closure rates were 25±1.5% and 34±2.9% for miR-221 and miR-222 inhibitors, respectively, versus 57±7% for pEX-5 (P<0.01 to 0.05) at 48 h; and 47±2.7% and 59±9.9% versus 100% (P<0.01) at 72 h. Similar findings for inhibition of migration were observed using a transwell assay. As shown in Figures 5C and D, cell migration was significantly decreased after transfection with miR-221 inhibitor or miR-222 inhibitor compared with in cells transfected with pEX-5 (P<0.01).


Down-regulation of mir-221 and mir-222 restrain prostate cancer cell proliferation and migration that is partly mediated by activation of SIRT1.

Yang X, Yang Y, Gan R, Zhao L, Li W, Zhou H, Wang X, Lu J, Meng QH - PLoS ONE (2014)

Effects of miR-221 inhibitor and miR-222 inhibitor on PC-3 cell migration.(A) Wound healing assay shows the closure rates of cells transfected with pEX-5 (empty vector plasmid), miR-221 inhibitor, or miR-222 inhibitor. (B) Quantitation of wound closure rates at different time points. (C) Transwell assay shows that the cells penetrated the insert membrane. (D) Quantitation of the number of cells that penetrated the insert membrane. Data represent the mean value ± SEM from three separate experiments. *,# P<0.05 vs pEX-5, **,## P<0.01 vs pEX-55).
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4043919&req=5

pone.0098833-g005: Effects of miR-221 inhibitor and miR-222 inhibitor on PC-3 cell migration.(A) Wound healing assay shows the closure rates of cells transfected with pEX-5 (empty vector plasmid), miR-221 inhibitor, or miR-222 inhibitor. (B) Quantitation of wound closure rates at different time points. (C) Transwell assay shows that the cells penetrated the insert membrane. (D) Quantitation of the number of cells that penetrated the insert membrane. Data represent the mean value ± SEM from three separate experiments. *,# P<0.05 vs pEX-5, **,## P<0.01 vs pEX-55).
Mentions: As shown in Figures 5A and B, the closure rates of the miR-221 inhibitor and miR-222 inhibitor groups were lower than was that of pEX-5 group. For instance, the closure rates were 25±1.5% and 34±2.9% for miR-221 and miR-222 inhibitors, respectively, versus 57±7% for pEX-5 (P<0.01 to 0.05) at 48 h; and 47±2.7% and 59±9.9% versus 100% (P<0.01) at 72 h. Similar findings for inhibition of migration were observed using a transwell assay. As shown in Figures 5C and D, cell migration was significantly decreased after transfection with miR-221 inhibitor or miR-222 inhibitor compared with in cells transfected with pEX-5 (P<0.01).

Bottom Line: MiR-221 and miR-222 were highly expressed in PC-3 cells compared with in LNCap cells.Cells transfected with siSIRT1 showed increased migration and a decreased apoptosis rate, but there was no significant effect on cell proliferation compared with the controls.These effects are potentially mediated by up-regulation of SIRT1.

View Article: PubMed Central - PubMed

Affiliation: Wenzhou Medical University School of Laboratory Medicine and Life Sciences, Wenzhou, Zhejiang, China.

ABSTRACT
Studies have shown that miR-221 and miR-222 are deregulated in many cancers, including prostate cancer. Nevertheless, the biological role and the underlying mechanisms of miR-221 and miR-222 in the pathogenesis of androgen-independent prostate cancer are still not clear. The proliferation, apoptosis, cell cycle distinction, and migration capacity of prostate cells were determined following transfection of miR-221 or miR-222 inhibitor. The biological impact and regulation of SIRT1 on prostate cancer cells were investigated. MiR-221 and miR-222 were highly expressed in PC-3 cells compared with in LNCap cells. After miR-221 or miR-222 expression was inhibited, the proliferation and migration rates of PC-3 cells decreased and the apoptosis rate increased. Moreover, SIRT1 protein was up-regulated in cells after they were transfected with miR-221 or miR-222 inhibitor. Cells transfected with siSIRT1 showed increased migration and a decreased apoptosis rate, but there was no significant effect on cell proliferation compared with the controls. There was a negative correlation between miR-221 or miR-222 and SIRT1, but no direct target relationship was identified. These data demonstrate that miR-221 and miR-222 are highly expressed in PC-3 cells. Their inhibition leads to reduced cell proliferation and migration and increased apoptosis in prostate cancer cells. These effects are potentially mediated by up-regulation of SIRT1.

Show MeSH
Related in: MedlinePlus