MiR-34a-3p alters proliferation and apoptosis of meningioma cells , javax.xml.bind.JAXBElement@3565bad6, and is directly targeting SMAD4, FRAT1 and BCL2. Werner, T. V, Hart, M., Nickels, R., Kim, Y., Menger, M. D, Bohle, R. M, Keller, A., Ludwig, N., & Meese, E. Aging, 9:932–954, March, 2017.
doi  abstract   bibtex   
Micro (mi)RNAs are short, noncoding RNAs and deregulation of miRNAs and their targets are implicated in tumor generation and progression in many cancers. Meningiomas are mostly benign, slow growing tumors of the central nervous system with a small percentage showing a malignant phenotype.Following prediction of potential targets of miR-34a-3p, , , and have been confirmed as targets by dual luciferase assays with co-expression of miR-34a-3p and reporter gene constructs containing the respective 3'UTRs. Disruption of the miR-34a-3p binding sites in the 3'UTRs resulted in loss of responsiveness to miR-34a-3p overexpression. In meningioma cells, overexpression of miR-34a-3p resulted in decreased protein levels of SMAD4, FRAT1 and BCL2, while inhibition of miR-34a-3p led to increased levels of these proteins as confirmed by Western blotting. Furthermore, deregulation of miR-34a-3p altered cell proliferation and apoptosis of meningioma cells .We show that , and are direct targets of miR-34a-3p and that deregulation of miR-34a-3p alters proliferation and apoptosis of meningioma cells . As part of their respective signaling pathways, which are known to play a role in meningioma genesis and progression, deregulation of , and might contribute to the aberrant activation of these signaling pathways leading to increased proliferation and inhibition of apoptosis in meningiomas.
@Article{Werner2017,
  author          = {Werner, Tamara V and Hart, Martin and Nickels, Ruth and Kim, Yoo-Jin and Menger, Michael D and Bohle, Rainer M and Keller, Andreas and Ludwig, Nicole and Meese, Eckart},
  title           = {MiR-34a-3p alters proliferation and apoptosis of meningioma cells , javax.xml.bind.JAXBElement@3565bad6, and is directly targeting SMAD4, FRAT1 and BCL2.},
  journal         = {Aging},
  year            = {2017},
  volume          = {9},
  pages           = {932--954},
  month           = mar,
  issn            = {1945-4589},
  abstract        = {Micro (mi)RNAs are short, noncoding RNAs and deregulation of miRNAs and their targets are implicated in tumor generation and progression in many cancers. Meningiomas are mostly benign, slow growing tumors of the central nervous system with a small percentage showing a malignant phenotype.Following   prediction of potential targets of miR-34a-3p,  ,  , and   have been confirmed as targets by dual luciferase assays with co-expression of miR-34a-3p and reporter gene constructs containing the respective 3'UTRs. Disruption of the miR-34a-3p binding sites in the 3'UTRs resulted in loss of responsiveness to miR-34a-3p overexpression. In meningioma cells, overexpression of miR-34a-3p resulted in decreased protein levels of SMAD4, FRAT1 and BCL2, while inhibition of miR-34a-3p led to increased levels of these proteins as confirmed by Western blotting. Furthermore, deregulation of miR-34a-3p altered cell proliferation and apoptosis of meningioma cells  .We show that  ,   and   are direct targets of miR-34a-3p and that deregulation of miR-34a-3p alters proliferation and apoptosis of meningioma cells  . As part of their respective signaling pathways, which are known to play a role in meningioma genesis and progression, deregulation of  ,   and   might contribute to the aberrant activation of these signaling pathways leading to increased proliferation and inhibition of apoptosis in meningiomas.},
  chemicals       = {BCL2 protein, human, FRAT1 protein, human, Intracellular Signaling Peptides and Proteins, MIRN34 microRNA, human, MicroRNAs, Proto-Oncogene Proteins, Proto-Oncogene Proteins c-bcl-2, Smad4 Protein},
  citation-subset = {IM},
  completed       = {2017-11-16},
  country         = {United States},
  doi             = {10.18632/aging.101201},
  issn-linking    = {1945-4589},
  issue           = {3},
  keywords        = {Apoptosis, genetics; Cell Line, Tumor; Cell Proliferation, genetics; Computer Simulation; Gene Expression Regulation, Neoplastic; Humans; Intracellular Signaling Peptides and Proteins, genetics, metabolism; Meningeal Neoplasms, genetics, metabolism, pathology; Meningioma, genetics, metabolism, pathology; MicroRNAs, genetics, metabolism; Proto-Oncogene Proteins, genetics, metabolism; Proto-Oncogene Proteins c-bcl-2, genetics, metabolism; Signal Transduction, genetics; Smad4 Protein, genetics, metabolism; BCL2; FRAT1; SMAD4; meningioma; miR-34a-3p},
  nlm-id          = {101508617},
  owner           = {NLM},
  pii             = {101201},
  pmc             = {PMC5391240},
  pmid            = {28340489},
  pubmodel        = {Print},
  pubstatus       = {ppublish},
  revised         = {2017-11-28},
}
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