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C-Myc negatively controls the tumor suppressor PTEN by upregulating miR-26a in glioblastoma multiforme cells

•The c-Myc oncogene directly upregulates miR-26a expression in GBM cells.•ChIP assays demonstrate that c-Myc interacts with the miR-26a promoter.•Luciferase reporter assays show that PTEN is a specific target of miR-26a.•C-Myc–miR-26a suppression of PTEN may regulate the PTEN/AKT pathway.•Overexpres... Full description

Journal Title: Biochemical and Biophysical Research Communications 08 November 2013, Vol.441(1), pp.186-190
Main Author: Guo, Pin
Other Authors: Nie, Quanmin , Lan, Jin , Ge, Jianwei , Qiu, Yongming , Mao, Qing
Format: Electronic Article Electronic Article
Language: English
Subjects:
Gbm
Bcl
Aml
ID: ISSN: 0006-291X ; E-ISSN: 1090-2104 ; DOI: 10.1016/j.bbrc.2013.10.034
Link: http://dx.doi.org/10.1016/j.bbrc.2013.10.034
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recordid: elsevier_sdoi_10_1016_j_bbrc_2013_10_034
title: C-Myc negatively controls the tumor suppressor PTEN by upregulating miR-26a in glioblastoma multiforme cells
format: Article
creator:
  • Guo, Pin
  • Nie, Quanmin
  • Lan, Jin
  • Ge, Jianwei
  • Qiu, Yongming
  • Mao, Qing
subjects:
  • C-Myc
  • Mir-26a
  • Pten
  • Proliferation
  • Glioblastoma Multiforme
  • Pten
  • Gbm
  • Mirna
  • 3′-Utr
  • Bcl
  • Aml
  • Cck-8
  • C-Myc
  • Mir-26a
  • Pten
  • Proliferation
  • Glioblastoma Multiforme
  • Biology
  • Chemistry
ispartof: Biochemical and Biophysical Research Communications, 08 November 2013, Vol.441(1), pp.186-190
description: •The c-Myc oncogene directly upregulates miR-26a expression in GBM cells.•ChIP assays demonstrate that c-Myc interacts with the miR-26a promoter.•Luciferase reporter assays show that PTEN is a specific target of miR-26a.•C-Myc–miR-26a suppression of PTEN may regulate the PTEN/AKT pathway.•Overexpression of c-Myc enhances the proliferative capacity of GBM cells. The c-Myc oncogene is amplified in many tumor types. It is an important regulator of cell proliferation and has been linked to altered miRNA expression, suggesting that c-Myc-regulated miRNAs might contribute to tumor progression. Although miR-26a has been reported to be upregulated in glioblastoma multiforme (GBM), the mechanism has not been established. We have shown that ectopic expression of miR-26a influenced cell proliferation by targeting PTEN, a tumor suppressor gene that is inactivated in many common malignancies, including GBM. Our findings suggest that c-Myc modulates genes associated with...
language: eng
source:
identifier: ISSN: 0006-291X ; E-ISSN: 1090-2104 ; DOI: 10.1016/j.bbrc.2013.10.034
fulltext: fulltext
issn:
  • 0006-291X
  • 0006291X
  • 1090-2104
  • 10902104
url: Link


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titleC-Myc negatively controls the tumor suppressor PTEN by upregulating miR-26a in glioblastoma multiforme cells
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ispartofBiochemical and Biophysical Research Communications, 08 November 2013, Vol.441(1), pp.186-190
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subjectC-Myc ; Mir-26a ; Pten ; Proliferation ; Glioblastoma Multiforme ; Pten ; Gbm ; Mirna ; 3′-Utr ; Bcl ; Aml ; Cck-8 ; C-Myc ; Mir-26a ; Pten ; Proliferation ; Glioblastoma Multiforme ; Biology ; Chemistry
description•The c-Myc oncogene directly upregulates miR-26a expression in GBM cells.•ChIP assays demonstrate that c-Myc interacts with the miR-26a promoter.•Luciferase reporter assays show that PTEN is a specific target of miR-26a.•C-Myc–miR-26a suppression of PTEN may regulate the PTEN/AKT pathway.•Overexpression of c-Myc enhances the proliferative capacity of GBM cells. The c-Myc oncogene is amplified in many tumor types. It is an important regulator of cell proliferation and has been linked to altered miRNA expression, suggesting that c-Myc-regulated miRNAs might contribute to tumor progression. Although miR-26a has been reported to be upregulated in glioblastoma multiforme (GBM), the mechanism has not been established. We have shown that ectopic expression of miR-26a influenced cell proliferation by targeting PTEN, a tumor suppressor gene that is inactivated in many common malignancies, including GBM. Our findings suggest that c-Myc modulates genes associated with...
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•The c-Myc oncogene directly upregulates miR-26a expression in GBM cells.•ChIP assays demonstrate that c-Myc interacts with the miR-26a promoter.•Luciferase reporter assays show that PTEN is a specific target of miR-26a.•C-Myc–miR-26a suppression of PTEN may regulate the PTEN/AKT pathway.•Overexpression of c-Myc enhances the proliferative capacity of GBM cells.

The c-Myc oncogene is amplified in many tumor types. It is an important regulator of cell proliferation and has been linked to altered miRNA expression, suggesting that c-Myc-regulated miRNAs might contribute to tumor progression. Although miR-26a has been reported to be upregulated in glioblastoma multiforme (GBM), the mechanism has not been established. We have shown that ectopic expression of miR-26a influenced cell proliferation by targeting PTEN, a tumor suppressor gene that is inactivated in many common malignancies, including GBM. Our findings suggest that c-Myc modulates genes associated with...

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•The c-Myc oncogene directly upregulates miR-26a expression in GBM cells.•ChIP assays demonstrate that c-Myc interacts with the miR-26a promoter.•Luciferase reporter assays show that PTEN is a specific target of miR-26a.•C-Myc–miR-26a suppression of PTEN may regulate the PTEN/AKT pathway.•Overexpression of c-Myc enhances the proliferative capacity of GBM cells.

The c-Myc oncogene is amplified in many tumor types. It is an important regulator of cell proliferation and has been linked to altered miRNA expression, suggesting that c-Myc-regulated miRNAs might contribute to tumor progression. Although miR-26a has been reported to be upregulated in glioblastoma multiforme (GBM), the mechanism has not been established. We have shown that ectopic expression of miR-26a influenced cell proliferation by targeting PTEN, a tumor suppressor gene that is inactivated in many common malignancies, including GBM. Our findings suggest that c-Myc modulates genes associated with...

pubElsevier Inc
doi10.1016/j.bbrc.2013.10.034
lad01Biochemical and Biophysical Research Communications
date2013-11-08