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MicroRNA 128a Increases Intracellular ROS Level by Targeting Bmi-1 and Inhibits Medulloblastoma Cancer Cell Growth by Promoting Senescence

Venkataraman, Sujatha, Alimova, Irina, Fan, Rong, Harris, Peter, Foreman, Nicholas, Vibhakar, Rajeev·2010·PLoS ONE
DOI 10.1371/journal.pone.0010748PMC PMC2888574
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Figure 1 Down regulation of microRNAs in medulloblastoma. A) MicroRNA heat map profiling of medulloblastoma patient samples and comparison to normal cerebellum. B) Repression of miR-125, miR-128, miR-139, let-7g and increased expression of miR17-5p in medulloblastoma cell lines. C) Relative expression of microRNAs in medulloblastoma patient samples.
Figure 1 Down regulation of microRNAs in medulloblastoma. A) MicroRNA heat map profiling of medulloblastoma patient samples and comparison to normal cerebellum. B) Repression of miR-125, miR-128, miR-139, let-7g and increased expression of miR17-5p in medulloblastoma cell lines. C) Relative expression of microRNAs in medulloblastoma patient samples.CC BY · PubMed Central
Figure 2 Inhibition of medulloblastoma cell growth by microRNA-128a. A) MiR-128a inhibits medulloblastoma cell proliferation as measured by MTT assay. (p<01) B) Number of Daoy cells as measured by trypan blue dye exclusion assay. C) Decreased colony formation in miR-128a transfected cells (top row is miR-128a vector, bottom row is control vector). D) Colony counts in triplicate of 2 independent experiments. (p<0.001)
Figure 2 Inhibition of medulloblastoma cell growth by microRNA-128a. A) MiR-128a inhibits medulloblastoma cell proliferation as measured by MTT assay. (p<01) B) Number of Daoy cells as measured by trypan blue dye exclusion assay. C) Decreased colony formation in miR-128a transfected cells (top row is miR-128a vector, bottom row is control vector). D) Colony counts in triplicate of 2 independent experiments. (p<0.001)CC BY · PubMed Central
Figure 3 Transfection of Daoy cells with miR-128a decreases Bmi-1 expression. A) MiR-128a target site in the Bmi-1 3′UTR. B) Luciferase reporter assays indicate that miR-128a functionally targets the wt Bmi-1 3′UTR, *p<0.01 C) Western blot analysis confirms that miR-128a, but not the control miR (CM), inhibits protein expression of Bmi-1 in medulloblastoma cells. D) Quantitation of Western blot bands. (p<0.01)
Figure 3 Transfection of Daoy cells with miR-128a decreases Bmi-1 expression. A) MiR-128a target site in the Bmi-1 3′UTR. B) Luciferase reporter assays indicate that miR-128a functionally targets the wt Bmi-1 3′UTR, *p<0.01 C) Western blot analysis confirms that miR-128a, but not the control miR (CM), inhibits protein expression of Bmi-1 in medulloblastoma cells. D) Quantitation of Western blot bands. (p<0.01)CC BY · PubMed Central
Figure 4 Growth inhibition signaling pathways modulated by miR-128a. A) Western blot analysis showed increased p16 expression in Daoy cells transfected with miR-128a compared to that of the control vector, pVETL. The level of p16 expression was completely inhibited in Daoy cells that were transfected with the Bmi-1 vector alone while modest inhibition was observed in cells co-transfected with miR-128a. B) Decreased E2F1 activity in Daoy cells transfected with miR-128a as measured by luciferase reporter assays. (p<0.01)
Figure 4 Growth inhibition signaling pathways modulated by miR-128a. A) Western blot analysis showed increased p16 expression in Daoy cells transfected with miR-128a compared to that of the control vector, pVETL. The level of p16 expression was completely inhibited in Daoy cells that were transfected with the Bmi-1 vector alone while modest inhibition was observed in cells co-transfected with miR-128a. B) Decreased E2F1 activity in Daoy cells transfected with miR-128a as measured by luciferase reporter assays. (p<0.01)CC BY · PubMed Central
Figure 5 Bmi-1 rescues miR-128a mediated growth arrest of medulloblastoma cells. A) Co-transfection of Daoy cells with miR-128a and Bmi-1 increased the number of colonies formed compared to that of miR-128a alone. B) Quantitative analysis of the number of colonies formed by Daoy cells after different transfections, including Bmi-1 that lacks its 3′UTR. pBABE-puro is a control vector for the full length Bmi-1. *p<0.05 for miR-128a vs. pVETL and **p<0.001 for miR-128a vs. miR-128a + Bmi-1.
Figure 5 Bmi-1 rescues miR-128a mediated growth arrest of medulloblastoma cells. A) Co-transfection of Daoy cells with miR-128a and Bmi-1 increased the number of colonies formed compared to that of miR-128a alone. B) Quantitative analysis of the number of colonies formed by Daoy cells after different transfections, including Bmi-1 that lacks its 3′UTR. pBABE-puro is a control vector for the full length Bmi-1. *p<0.05 for miR-128a vs. pVETL and **p<0.001 for miR-128a vs. miR-128a + Bmi-1.CC BY · PubMed Central
Figure 6 MiR-128a increases intracellular ROS by targeting Bmi-1. A) Increased superoxide radical formation in Daoy cells that were transfected with miR-128a as detected using EPR spectra of the DMPO-OH spin adduct (closed circles in (ii)). The spectra collected are a signal average of 15 scans. The 1∶2∶2∶1(closed circles) quartet signal seen is due to the formation of DMPO-OH. The cells treated with miR-128a have ∼3 fold increase in ROS signal intensity (ii) as compared to the empty vector (i). Co-transfection of cells with miR-128a and Bmi-1 resulted in a decreased ROS level compared to that of miR-128a alone (iii). The treatment of SOD in miR-128a-transfected cells abolished the signals showing that the radical formed is mainly superoxide (iv). B) The quantitative analysis of EPR peak height normalized to cell number. *p<0.05 miR128a vs. pVETL and miR-128a + SOD.
Figure 6 MiR-128a increases intracellular ROS by targeting Bmi-1. A) Increased superoxide radical formation in Daoy cells that were transfected with miR-128a as detected using EPR spectra of the DMPO-OH spin adduct (closed circles in (ii)). The spectra collected are a signal average of 15 scans. The 1∶2∶2∶1(closed circles) quartet signal seen is due to the formation of DMPO-OH. The cells treated with miR-128a have ∼3 fold increase in ROS signal intensity (ii) as compared to the empty vector (i). Co-transfection of cells with miR-128a and Bmi-1 resulted in a decreased ROS level compared to that of miR-128a alone (iii). The treatment of SOD in miR-128a-transfected cells abolished the signals showing that the radical formed is mainly superoxide (iv). B) The quantitative analysis of EPR peak height normalized to cell number. *p<0.05 miR128a vs. pVETL and miR-128a + SOD.CC BY · PubMed Central
Figure 7 MiR-128a promotes senescence in medulloblastoma cells. A) MiR-128a induces senescence in medulloblastoma cells as detected by SA-beta galactosidase staining (dark blue cells; examples indicated by red arrows). B) Cell counts per High Powered Field of β-gal positive cells in control vector (pVETL) or miR-128a transfected cells, *p = 0.003. C) Western blot analysis showing increased level of H3K9me2 protein in Daoy cells transfected with miR-128a when compared to the empty vector. Actin is used as an internal control.
Figure 7 MiR-128a promotes senescence in medulloblastoma cells. A) MiR-128a induces senescence in medulloblastoma cells as detected by SA-beta galactosidase staining (dark blue cells; examples indicated by red arrows). B) Cell counts per High Powered Field of β-gal positive cells in control vector (pVETL) or miR-128a transfected cells, *p = 0.003. C) Western blot analysis showing increased level of H3K9me2 protein in Daoy cells transfected with miR-128a when compared to the empty vector. Actin is used as an internal control.CC BY · PubMed Central

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Metadata

Authors
Venkataraman, S., Alimova, I., Fan, R., Harris, P., Foreman, N., & Vibhakar, R.
Venue
PLoS ONE
Publisher
Public Library of Science (PLoS)
Published
2010-06-21
Volume
5
Issue
6
Pages
e10748
ISSN
1932-6203
DOI
10.1371/journal.pone.0010748
PMC
PMC2888574
Cited by
156
References
6
Language
en
Licence
creativecommons.org/licenses/by/4.0/ (unspecified)

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