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MicroRNA-128 coordinately targets Polycomb Repressor Complexes in glioma stem cells
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In the citing paper
“Notably, the level of miR-128-3p was significantly reduced in the brain tissue of young, pre-symptomatic mice genetically modified to develop glioblastomas but not in the brain of wild-type mice, demonstrating that the miR-128-3p suppression is an early event during gliomagenesis.77”
From MiR-128-3p – a gray eminence of the human central nervous system (2024) · cites this paper as [77]
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In the citing paper
“MiR-128-3p was found to be a potent regulator of the expression and activity of proteins forming polycomb repressive complexes (PRCs).”
From MiR-128-3p – a gray eminence of the human central nervous system (2024) · cites this paper as [77]
The cited source says what the claim attributes to it.
In the citing paper
“Thus, the activation of PRCs, evident from increased expression of BMI1 and SUZ12,77 contributed to the radio-resistance of tumor cells,137,138 including glioblastoma.139,140”
From MiR-128-3p – a gray eminence of the human central nervous system (2024) · cites this paper as [77]
In the citing paper
“As the functional consequences of miR-128-3p,77,126 re-establishment and repression of PRCs subunits, pronounced alterations in histone modifications,77 as well as loss of stem-like features by GSCs, were observed in vitro and in vivo, as clearly shown by down-regulation of CD133 (Prominin-1) expression.77,126”
From MiR-128-3p – a gray eminence of the human central nervous system (2024) · cites this paper as [77]
In the citing paper
“As the functional consequences of miR-128-3p,77,126 re-establishment and repression of PRCs subunits, pronounced alterations in histone modifications,77 as well as loss of stem-like features by GSCs, were observed in vitro and in vivo, as clearly shown by down-regulation of CD133 (Prominin-1) expression.77,126”
From MiR-128-3p – a gray eminence of the human central nervous system (2024) · cites this paper as [77]
In the citing paper
“where a reduced level of miR-128-3p was correlated with worse patient outcomes.77,78,79”
From MiR-128-3p – a gray eminence of the human central nervous system (2024) · cites this paper as [77]
In the citing paper
“Several studies showed that up-regulation of miR-128-3p profoundly reduced the expression of core protein components of PRC1 and PRC2: BMI-1 (Polycomb complex protein BMI-1)77,126,127 and SUZ12 (Polycomb protein SUZ12),77,128,129 respectively.”
From MiR-128-3p – a gray eminence of the human central nervous system (2024) · cites this paper as [77]
In the citing paper
“The reintroduction of miR-128-3p77,126 significantly inhibited the radiation-induced expression of PRC subunits and consequently enhanced the radiosensitivity of GSCs accompanied by substantial DNA damage.77,126”
From MiR-128-3p – a gray eminence of the human central nervous system (2024) · cites this paper as [77]
In the citing paper
“Crucially, many microRNAs coordinately target numerous factors from the same pathway, thus circumventing their physiological redundancy, e.g., miR-128-3p targeting several vital players of the PRC pathway.77,130”
From MiR-128-3p – a gray eminence of the human central nervous system (2024) · cites this paper as [77]
In the citing paper
“More importantly, EVs originating from non-malignant cells do not propagate pro-tumorigenic signals to cancer cells and are not toxic to normal cells and tissues.69,77,126,130,221”
From MiR-128-3p – a gray eminence of the human central nervous system (2024) · cites this paper as [77]
In the citing paper
“Conversely, up-regulation of PRC components and PRC-dependent chromatin modifications that increased clonogenic potential were observed in both mouse and human non-malignant NSCs upon miR-128-3p knockdown.77”
From MiR-128-3p – a gray eminence of the human central nervous system (2024) · cites this paper as [77]
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Citations
Cites
The Polycomb complex PRC2 and its mark in life
Margueron, R., & Reinberg, D. (2011) · Nature · doi:10.1038/nature09784 · Cited by 3,347
Astrocytes from familial and sporadic ALS patients are toxic to motor neurons
Haidet-Phillips, A. M., Hester, M. E., Miranda, C. J., Meyer, K., Braun, L., Frakes, A., Song, S., Likhite, S., Murtha, M. J., Foust, K. D., et al. (2011) · Nature Biotechnology · doi:10.1038/nbt.1957 · Cited by 782
Regulation of miRNA expression during neural cell specification
Smirnova, L., Gräfe, A., Seiler, A., Schumacher, S., Nitsch, R., & Wulczyn, F. G. (2005) · European Journal of Neuroscience · doi:10.1111/j.1460-9568.2005.03978.x · Cited by 707
Stock, J. K., Giadrossi, S., Casanova, M., Brookes, E., Vidal, M., Koseki, H., Brockdorff, N., Fisher, A. G., & Pombo, A. (2007) · Nature Cell Biology · doi:10.1038/ncb1663 · Cited by 650
Chou, D. M., Adamson, B., Dephoure, N. E., Tan, X., Nottke, A. C., Hurov, K. E., Gygi, S. P., Colaiácovo, M. P., & Elledge, S. J. (2010) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1012946107 · Cited by 529 · cited 1×
“PRCs have been shown to be activated by radiation, as they play a significant role in DNA repair.(31,33,35,37) First, we established that the response of glioblastoma cells to radiation involves a dose-dependent increase in the expression of the Polycomb genes SUZ12 and BMI1 by quantitative RT-PCR (Fig.”
BackgroundIliopoulos, D., Lindahl-Allen, M., Polytarchou, C., Hirsch, H. A., Tsichlis, P. N., & Struhl, K. (2010) · Molecular Cell · doi:10.1016/j.molcel.2010.08.013 · Cited by 399
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Research works printed but not linked: 65
- Davis, 2001, Current epidemiological trends and surveillance issues in brain tumors, Expert Rev Anticancer Ther, 1, 395, 10.1586/14737140.1.3.395 · DOI
- Stupp, 2005, Radiotherapy plus concomitant and adjuvant temozolomide for glioblastoma, N Engl J Med, 352, 987, 10.1056/NEJMoa043330 · DOI · Paper page
- Chen, 2012, Malignant glioma: lessons from genomics, mouse models, and stem cells, Cell, 149, 36, 10.1016/j.cell.2012.03.009 · DOI
- Guerrero-Cazares, 2012, Stem cells in gliomas, Handb Clin Neurol, 104, 63, 10.1016/B978-0-444-52138-5.00006-2 · DOI
- Nduom, 2012, Glioblastoma cancer stem-like cells: implications for pathogenesis and treatment, Cancer J, 18, 100, 10.1097/PPO.0b013e3182452e0d · DOI
- Singh, 2004, Identification of human brain tumour initiating cells, Nature, 432, 396, 10.1038/nature03128 · DOI
- Piccirillo, 2006, Bone morphogenetic proteins inhibit the tumorigenic potential of human brain tumour-initiating cells, Nature, 444, 761, 10.1038/nature05349 · DOI
- Godlewski, 2010, MicroRNAs and glioblastoma; the stem cell connection, Cell Death Differ, 17, 221, 10.1038/cdd.2009.71 · DOI · Paper page
- Iorio, 2012, MicroRNA dysregulation in cancer: diagnostics, monitoring and therapeutics. A comprehensive review, EMBO Mol Med, 4, 143, 10.1002/emmm.201100209 · DOI
- Lawler, 2009, Emerging functions of microRNAs in glioblastoma, J Neurooncol, 92, 297, 10.1007/s11060-009-9843-2 · DOI
- Lovat, 2011, MicroRNAs in the pathogenesis of cancer, Semin Oncol, 38, 724, 10.1053/j.seminoncol.2011.08.006 · DOI
- Sana, 2011, MicroRNAs and glioblastoma: roles in core signalling pathways and potential clinical implications, J Cell Mol Med, 15, 1636, 10.1111/j.1582-4934.2011.01317.x · DOI
- Bartel, 2009, MicroRNAs: target recognition and regulatory functions, Cell, 136, 215, 10.1016/j.cell.2009.01.002 · DOI · Paper page
- Ciafre, 2005, Extensive modulation of a set of microRNAs in primary glioblastoma, Biochem Biophys Res Commun, 334, 1351, 10.1016/j.bbrc.2005.07.030 · DOI · Paper page
- 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
- Rajasekhar, 2007, Concise review: roles of polycomb group proteins in development and disease: a stem cell perspective, Stem Cells, 25, 2498, 10.1634/stemcells.2006-0608 · DOI
- Prezioso, 2011, Polycomb proteins in mammalian cell differentiation and plasticity, FEBS Lett, 585, 2067, 10.1016/j.febslet.2011.04.062 · DOI
- Aldiri, 2012, PRC2 during vertebrate organogenesis: a complex in transition, Dev Biol, 367, 91, 10.1016/j.ydbio.2012.04.030 · DOI
- Jones, 2010, Polycomb repressive complex 2 in embryonic stem cells: an overview, Protein Cell, 1, 1056, 10.1007/s13238-010-0142-7 · DOI
- Pasini, 2004, Polycomb group proteins in cell cycle progression and cancer, Cell Cycle, 3, 396, 10.4161/cc.3.4.773 · DOI · Paper page
- Richly, 2011, Roles of the Polycomb group proteins in stem cells and cancer, Cell Death Dis, 2, e204, 10.1038/cddis.2011.84 · DOI · Paper page
- Sauvageau, 2010, Polycomb group proteins: multi-faceted regulators of somatic stem cells and cancer, Cell Stem Cell, 7, 299, 10.1016/j.stem.2010.08.002 · DOI · Paper page
- Wu, 2011, Epithelial-mesenchymal transition and cancer stemness: the Twist1-Bmi1 connection, Biosci Rep, 31, 449, 10.1042/BSR20100114 · DOI
- Hayry, 2008, Copy number alterations of the polycomb gene BMI1 in gliomas, Acta Neuropathol, 116, 97, 10.1007/s00401-008-0376-0 · DOI · Paper page
- Crea, 2010, Clinical significance of Polycomb gene expression in brain tumors, Mol Cancer, 9, 265, 10.1186/1476-4598-9-265 · DOI · Paper page
- Orzan, 2011, Enhancer of Zeste 2 (EZH2) is up-regulated in malignant gliomas and in glioma stem-like cells, Neuropathol Appl Neurobiol, 37, 381, 10.1111/j.1365-2990.2010.01132.x · DOI
- Abdouh, 2009, BMI1 sustains human glioblastoma multiforme stem cell renewal, J Neurosci, 29, 8884, 10.1523/JNEUROSCI.0968-09.2009 · DOI
- Suva, 2009, EZH2 is essential for glioblastoma cancer stem cell maintenance, Cancer Res, 69, 9211, 10.1158/0008-5472.CAN-09-1622 · DOI
- Facchino, 2011, Brain cancer stem cells: current status on glioblastoma multiforme, Cancers, 3, 1777, 10.3390/cancers3021777 · DOI
- Gieni, 2011, Polycomb group proteins in the DNA damage response: a link between radiation resistance and “stemness”, Cell Cycle, 10, 883, 10.4161/cc.10.6.14907 · DOI · Paper page
- Liu, 2012, Bmi-1 induces radioresistance in MCF-7 mammary carcinoma cells, Oncol Rep, 27, 1116, 10.3892/or.2011.1615 · DOI · Paper page
- Facchino, 2010, BMI1 confers radioresistance to normal and cancerous neural stem cells through recruitment of the DNA damage response machinery, J Neurosci, 30, 10096, 10.1523/JNEUROSCI.1634-10.2010 · DOI · Paper page
- Li, 2010, Oncoprotein Bmi-1 renders apoptotic resistance to glioma cells through activation of the IKK-nuclear factor-kappaB pathway, Am J Pathol, 176, 699, 10.2353/ajpath.2010.090502 · DOI · Paper page
- Ismail, 2010, BMI1-mediated histone ubiquitylation promotes DNA double-strand break repair, J Cell Biol, 191, 45, 10.1083/jcb.201003034 · DOI · Paper page
- Ginjala, 2011, BMI1 is recruited to DNA breaks and contributes to DNA damage-induced H2A ubiquitination and repair, Mol Cell Biol, 31, 1972, 10.1128/MCB.00981-10 · DOI · Paper page
- He, 2009, Bmi-1 over-expression in neural stem/progenitor cells increases proliferation and neurogenesis in culture but has little effect on these functions in vivo, Dev Biol, 328, 257, 10.1016/j.ydbio.2009.01.020 · DOI
- Pasini, 2004, Suz12 is essential for mouse development and for EZH2 histone methyltransferase activity, EMBO J, 23, 4061, 10.1038/sj.emboj.7600402 · DOI
- Singh, 2003, Identification of a cancer stem cell in human brain tumors, Cancer Res, 63, 5821
- Pollard, 2009, Glioma stem cell lines expanded in adherent culture have tumor-specific phenotypes and are suitable for chemical and genetic screens, Cell Stem Cell, 4, 568, 10.1016/j.stem.2009.03.014 · DOI · Paper page
- Nakano, 2011, Siomycin A targets brain tumor stem cells partially through a MELK-mediated pathway, Neuro Oncol, 13, 622, 10.1093/neuonc/nor023 · DOI
- Johnson, 1998, Applied Multivariate Statistical Analysis
- The Cancer Genome Atlas Research Network, 2008, Comprehensive genomic characterization defines human glioblastoma genes and core pathways, Nature, 455, 1061, 10.1038/nature07385 · DOI · Paper page
- Bracken, 2006, Genome-wide mapping of Polycomb target genes unravels their roles in cell fate transitions, Genes Dev, 20, 1123, 10.1101/gad.381706 · DOI
- Fasano, 2007, shRNA knockdown of Bmi-1 reveals a critical role for p21-Rb pathway in NSC self-renewal during development, Cell Stem Cell, 1, 87, 10.1016/j.stem.2007.04.001 · DOI
- Kwon, 2008, Pten haploinsufficiency accelerates formation of high-grade astrocytomas, Cancer Res, 68, 3286, 10.1158/0008-5472.CAN-07-6867 · DOI
- Zhu, 2005, Early inactivation of p53 tumor suppressor gene cooperating with NF1 loss induces malignant astrocytoma, Cancer Cell, 8, 119, 10.1016/j.ccr.2005.07.004 · DOI
- Alcantara Llaguno, 2009, Malignant astrocytomas originate from neural stem/progenitor cells in a somatic tumor suppressor mouse model, Cancer Cell, 15, 45, 10.1016/j.ccr.2008.12.006 · DOI · Paper page
- Leeb, 2010, Polycomb complexes act redundantly to repress genomic repeats and genes, Genes Dev, 24, 265, 10.1101/gad.544410 · DOI · Paper page
- Beier, 2011, Chemoresistance of glioblastoma cancer stem cells—much more complex than expected, Mol Cancer, 10, 128, 10.1186/1476-4598-10-128 · DOI
- Burkhardt, 2011, Neural stem cells and glioma stem-like cells respond differently to chemotherapeutic drugs: selectivity at the cellular level, Neurosurgery, 68, N21, 10.1227/01.neu.0000398212.65736.e1 · DOI
- Mannino, 2011, Radioresistance of glioma stem cells: intrinsic characteristic or property of the ‘microenvironment-stem cell unit’?, Mol Oncol, 5, 374, 10.1016/j.molonc.2011.05.001 · DOI
- Bao, 2006, Glioma stem cells promote radioresistance by preferential activation of the DNA damage response, Nature, 444, 756, 10.1038/nature05236 · DOI
- Bleau, 2009, PTEN/PI3K/Akt pathway regulates the side population phenotype and ABCG2 activity in glioma tumor stem-like cells, Cell Stem Cell, 4, 226, 10.1016/j.stem.2009.01.007 · DOI
- Nikaki, 2012, Role of microRNAs in gliomagenesis: targeting miRNAs in glioblastoma multiforme therapy, Expert Opin Investig Drugs, 21, 1475, 10.1517/13543784.2012.710199 · DOI
- Papagiannakopoulos, 2012, Pro-neural miR-128 is a glioma tumor suppressor that targets mitogenic kinases, Oncogene, 31, 1884, 10.1038/onc.2011.380 · DOI · Paper page
- Zhang, 2009, MicroRNA-128 inhibits glioma cells proliferation by targeting transcription factor E2F3a, J Mol Med (Berl), 87, 43, 10.1007/s00109-008-0403-6 · DOI · Paper page
- Shi, 2012, MiR-128 inhibits tumor growth and angiogenesis by targeting p70S6K1, PLoS One, 7, e32709, 10.1371/journal.pone.0032709 · DOI
- Qian, 2012, Loss of SNAIL regulated miR-128–2 on chromosome 3p22.3 targets multiple stem cell factors to promote transformation of mammary epithelial cells, Cancer Res, 72, 6036, 10.1158/0008-5472.CAN-12-1507 · DOI
- Arima, 2010, Decreased expression of neurofibromin contributes to epithelial-mesenchymal transition in neurofibromatosis type 1, Exp Dermatol, 19, e136, 10.1111/j.1600-0625.2009.01017.x · DOI
- Lim, 2010, p53 inhibits tumor cell invasion via the degradation of snail protein in hepatocellular carcinoma, FEBS Lett, 584, 2231, 10.1016/j.febslet.2010.04.006 · DOI
- Kurrey, 2009, Snail and Slug mediate radioresistance and chemoresistance by antagonizing p53-mediated apoptosis and acquiring a stem-like phenotype in ovarian cancer cells, Stem Cells, 27, 2059, 10.1002/stem.154 · DOI · Paper page
- Brabletz, 2012, MiR-34 and SNAIL: another double-negative feedback loop controlling cellular plasticity/EMT governed by p53, Cell Cycle, 11, 215, 10.4161/cc.11.2.18900 · DOI
- Li, 2009, MicroRNA-34a inhibits glioblastoma growth by targeting multiple oncogenes, Cancer Res, 69, 7569, 10.1158/0008-5472.CAN-09-0529 · DOI · Paper page
- Silber, 2012, miR-34a repression in proneural malignant gliomas upregulates expression of its target PDGFRA and promotes tumorigenesis, PLoS One, 7, e33844, 10.1371/journal.pone.0033844 · DOI
- Bader, 2010, The promise of microRNA replacement therapy, Cancer Res, 70, 7027, 10.1158/0008-5472.CAN-10-2010 · DOI
Cited by
Sorted by citations
Adlakha, Y. K., & Saini, N. (2014) · Molecular Cancer · doi:10.1186/1476-4598-13-33 · Cited by 213
MiR-128-3p – a gray eminence of the human central nervous system
Kiel, K., Król, S. K., Bronisz, A., & Godlewski, J. (2024) · Molecular Therapy Nucleic Acids · doi:10.1016/j.omtn.2024.102141 · Cited by 15
Self-citation
Metadata
- Authors
- Peruzzi, P., Bronisz, A., Nowicki, M. O., Wang, Y., Ogawa, D., Price, R., Nakano, I., Kwon, C.-H., Hayes, J., Lawler, S. E., Ostrowski, M. C., Chiocca, E. A., & Godlewski, J.
- Venue
- Neuro-Oncology
- Publisher
- Oxford University Press (OUP)
- Published
- 2013-06-03
- Volume
- 15
- Issue
- 9
- Pages
- 1212-1224
- ISSN
- 1523-5866
- 1522-8517
- Cited by
- 97
- References
- 6
- Language
- en
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