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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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Citations

Cites

Research works printed but not linked: 32

  1. JT Rutka, 2004, Advances in the treatment of pediatric brain tumors., Expert Rev Neurother, 4, 879, 10.1586/14737175.4.5.879 · DOI
  2. RK Mulhern, 2005, Neurocognitive consequences of risk-adapted therapy for childhood medulloblastoma., J Clin Oncol, 23, 5511, 10.1200/JCO.2005.00.703 · DOI
  3. SK Singh, 2004, Identification of human brain tumour initiating cells., Nature, 432, 396, 10.1038/nature03128 · DOI
  4. R Wechsler-Reya, 2001, The developmental biology of brain tumors., Annu Rev Neurosci, 24, 385, 10.1146/annurev.neuro.24.1.385 · DOI
  5. JB Rubin, 2002, Medulloblastoma: a problem of developmental biology., Cancer Cell, 2, 7, 10.1016/S1535-6108(02)00090-9 · DOI
  6. A Lee, 2005, Isolation of neural stem cells from the postnatal cerebellum., Nat Neurosci, 8, 723, 10.1038/nn1473 · DOI
  7. S Marino, 2005, Medulloblastoma: developmental mechanisms out of control., Trends Mol Med, 11, 17, 10.1016/j.molmed.2004.11.008 · DOI
  8. E Ferretti, 2009, MicroRNA profiling in human medulloblastoma., Int J Cancer, 124, 568, 10.1002/ijc.23948 · DOI
  9. PA Northcott, 2009, The miR-17/92 polycistron is up-regulated in sonic hedgehog-driven medulloblastomas and induced by N-myc in sonic hedgehog-treated cerebellar neural precursors., Cancer Res, 69, 3249, 10.1158/0008-5472.CAN-08-4710 · DOI
  10. J Pierson, 2008, Regulation of cyclin dependent kinase 6 by microRNA 124 in medulloblastoma., J Neurooncol, 90, 1, 10.1007/s11060-008-9624-3 · DOI · Paper page
  11. T Du, 2005, microPrimer: the biogenesis and function of microRNA., Development, 132, 4645, 10.1242/dev.02070 · DOI
  12. AJ Giraldez, 2005, MicroRNAs regulate brain morphogenesis in zebrafish., Science, 308, 833, 10.1126/science.1109020 · DOI · Paper page
  13. L He, 2005, A microRNA polycistron as a potential human oncogene., Nature, 435, 828, 10.1038/nature03552 · DOI
  14. S Costinean, 2006, Pre-B cell proliferation and lymphoblastic leukemia/high-grade lymphoma in E(mu)-miR155 transgenic mice., Proc Natl Acad Sci U S A, 103, 7024, 10.1073/pnas.0602266103 · DOI
  15. J Lu, 2005, MicroRNA expression profiles classify human cancers., Nature, 435, 834, 10.1038/nature03702 · DOI
  16. MS Kumar, 2007, Impaired microRNA processing enhances cellular transformation and tumorigenesis., Nat Genet, 39, 673, 10.1038/ng2003 · DOI
  17. MF Corsten, 2007, MicroRNA-21 knockdown disrupts glioma growth in vivo and displays synergistic cytotoxicity with neural precursor cell delivered S-TRAIL in human gliomas., Cancer Res, 67, 8994, 10.1158/0008-5472.CAN-07-1045 · DOI · Paper page
  18. J Silber, 2008, miR-124 and miR-137 inhibit proliferation of glioblastoma multiforme cells and induce differentiation of brain tumor stem cells., BMC Med, 6, 14, 10.1186/1741-7015-6-14 · DOI · Paper page
  19. T Uziel, 2009, The miR-17∼92 cluster collaborates with the Sonic Hedgehog pathway in medulloblastoma., Proc Natl Acad Sci U S A, 106, 2812, 10.1073/pnas.0809579106 · DOI
  20. MC Thompson, 2006, Genomics identifies medulloblastoma subgroups that are enriched for specific genetic alterations., J Clin Oncol, 24, 1924, 10.1200/JCO.2005.04.4974 · DOI
  21. A Grimson, 2007, MicroRNA Targeting Specificity in Mammals: Determinants beyond Seed Pairing., Mol Cell, 27, 91, 10.1016/j.molcel.2007.06.017 · DOI · Paper page
  22. J Godlewski, 2008, Targeting of the Bmi-1 oncogene/stem cell renewal factor by microRNA-128 inhibits glioma proliferation and self-renewal., Cancer Res, 68, 9125, 10.1158/0008-5472.CAN-08-2629 · DOI · Paper page
  23. AV Molofsky, 2003, Bmi-1 dependence distinguishes neural stem cell self-renewal from progenitor proliferation., Nature, 425, 962, 10.1038/nature02060 · DOI
  24. C Leung, 2004, Bmi1 is essential for cerebellar development and is overexpressed in human medulloblastomas., Nature, 428, 337, 10.1038/nature02385 · DOI
  25. D Mihic-Probst, 2007, Consistent expression of the stem cell renewal factor BMI-1 in primary and metastatic melanoma., Int J Cancer, 121, 1764, 10.1002/ijc.22891 · DOI
  26. AV Molofsky, 2005, Bmi-1 promotes neural stem cell self-renewal and neural development but not mouse growth and survival by repressing the p16Ink4a and p19Arf senescence pathways., Genes Dev, 19, 1432, 10.1101/gad.1299505 · DOI
  27. T Finkel, 1999, Signal transduction by reactive oxygen species in non-phagocytic cells., J Leukoc Biol, 65, 337, 10.1002/jlb.65.3.337 · DOI
  28. GM Rosen, 1984, Detection of superoxide generated by endothelial cells., Proc Natl Acad Sci U S A, 81, 7269, 10.1073/pnas.81.23.7269 · DOI
  29. T Lu, 2008, Free radicals and senescence., Exp Cell Res, 314, 1918, 10.1016/j.yexcr.2008.01.011 · DOI · Paper page
  30. YS Song, 2005, Dinstinct ROS and biochemical profiles in cells undergoing DNA damage-induced senescence and apoptosis., Mech Ageing Dev, 126, 580, 10.1016/j.mad.2004.11.008 · DOI
  31. E Hara, 1996, Regulation of p16CDKN2 expression and its implications for cell immortalization and senescence., Mol Cell Biol, 16, 859, 10.1128/MCB.16.3.859 · DOI · Paper page
  32. R Vibhakar, 2007, Dickkopf-1 is an epigenetically silenced candidate tumor suppressor gene in medulloblastoma., Neuro-oncol, 9, 135, 10.1215/15228517-2006-038 · DOI

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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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