English
 
Help Privacy Policy Disclaimer
  Advanced SearchBrowse

Item

ITEM ACTIONSEXPORT
  MiR-133b Targets Antiapoptotic Genes and Enhances Death Receptor-Induced Apoptosis

Patron, J. P., Fendler, A., Bild, M., Jung, U., Müller, H., Arntzen, M. O., et al. (2012). MiR-133b Targets Antiapoptotic Genes and Enhances Death Receptor-Induced Apoptosis. PLoS ONE, 7(4): e35345. doi:10.1371/journal.pone.0035345.

Item is

Basic

show hide
Genre: Journal Article
Alternative Title : PLoS One

Files

show Files
hide Files
:
PLoS_One_2012_7_e35345.pdf (Publisher version), 2MB
Name:
PLoS_One_2012_7_e35345.pdf
Description:
-
Visibility:
Public
MIME-Type / Checksum:
application/pdf / [MD5]
Technical Metadata:
Copyright Date:
-
Copyright Info:
Copyright Patron et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
License:
-

Locators

show

Creators

show
hide
 Creators:
Patron, Juan Pablo1, Author              
Fendler, Annika, Author
Bild, Matthias1, Author              
Jung, Ulrike1, Author              
Müller, Henrik1, Author              
Arntzen, Magnus O., Author
Piso, Chloe1, Author              
Stephan, Carsten, Author
Thiede, Bernd2, Author
Mollenkopf, Hans-Joachim3, Author              
Jung, Klaus, Author
Kaufmann, Stefan H. E.1, Author              
Schreiber, Joerg1, Author              
Affiliations:
1Department of Immunology, Max Planck Institute for Infection Biology, Max Planck Society, ou_1664146              
2External Organizations, ou_persistent22              
3Core Facilities / Microarray, Max Planck Institute for Infection Biology, Max Planck Society, ou_1664141              

Content

show
hide
Free keywords: -
 Abstract: Despite the importance of microRNAs (miRs) for regulation of the delicate balance between cell proliferation and death, evidence for their specific involvement during death receptor (DR)-mediated apoptosis is scarce. Transfection with miR-133b rendered resistant HeLa cells sensitive to tumor necrosis factor-alpha (TNF alpha)-induced cell death. Similarly, miR-133b caused exacerbated proapoptotic responses to TNF-related apoptosis-inducing ligand (TRAIL) or an activating antibody to Fas/CD95. Comprehensive analysis, encompassing global RNA or protein expression profiling performed by microarray experiments and pulsed stable isotope labeling with amino acids in cell culture (pSILAC), led to the discovery of the antiapoptotic protein Fas apoptosis inhibitory molecule (FAIM) as immediate miR-133b target. Moreover, miR-133b impaired the expression of the detoxifying protein glutathione-S-transferase pi (GSTP1). Expression of miR-133b in tumor specimens of prostate cancer patients was significantly downregulated in 75% of the cases, when compared with matched healthy tissue. Furthermore, introduction of synthetic miR-133b into an ex-vivo model of prostate cancer resulted in impaired proliferation and cellular metabolic activity. PC3 cells were also sensitized to apoptotic stimuli after transfection with miR-133b similar to HeLa cells. These data reveal the ability of a single miR to influence major apoptosis pathways, suggesting an essential role for this molecule during cellular transformation, tumorigenesis and tissue homeostasis.

Details

show
hide
Language(s):
 Dates: 2012-04-20
 Publication Status: Published in print
 Pages: -
 Publishing info: -
 Table of Contents: -
 Rev. Type: Peer
 Identifiers: eDoc: 611217
ISI: 000305339200058
DOI: 10.1371/journal.pone.0035345
 Degree: -

Event

show

Legal Case

show

Project information

show

Source 1

show
hide
Title: PLoS ONE
  Alternative Title : PLoS One
Source Genre: Journal
 Creator(s):
Affiliations:
Publ. Info: -
Pages: - Volume / Issue: 7 (4) Sequence Number: e35345 Start / End Page: - Identifier: ISSN: 1932-6203