MiR-133b targets antiapoptotic genes and enhances death receptor-induced apoptosis.

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 necrosi...

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Autores principales:	Juan P Patron, Annika Fendler, Matthias Bild, Ulrike Jung, Henrik Müller, Magnus Ø Arntzen, Chloe Piso, Carsten Stephan, Bernd Thiede, Hans-Joachim Mollenkopf, Klaus Jung, Stefan H E Kaufmann, Jörg Schreiber
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2012
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/68eeae15a69047a5905ae63710d8d6e6
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spelling	oai:doaj.org-article:68eeae15a69047a5905ae63710d8d6e62021-11-18T07:21:32ZMiR-133b targets antiapoptotic genes and enhances death receptor-induced apoptosis.1932-620310.1371/journal.pone.0035345https://doaj.org/article/68eeae15a69047a5905ae63710d8d6e62012-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/22532850/?tool=EBIhttps://doaj.org/toc/1932-6203Despite 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 (TNFα)-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.Juan P PatronAnnika FendlerMatthias BildUlrike JungHenrik MüllerMagnus Ø ArntzenChloe PisoCarsten StephanBernd ThiedeHans-Joachim MollenkopfKlaus JungStefan H E KaufmannJörg SchreiberPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 7, Iss 4, p e35345 (2012)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Juan P Patron Annika Fendler Matthias Bild Ulrike Jung Henrik Müller Magnus Ø Arntzen Chloe Piso Carsten Stephan Bernd Thiede Hans-Joachim Mollenkopf Klaus Jung Stefan H E Kaufmann Jörg Schreiber MiR-133b targets antiapoptotic genes and enhances death receptor-induced apoptosis.
description	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 (TNFα)-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.
format	article
author	Juan P Patron Annika Fendler Matthias Bild Ulrike Jung Henrik Müller Magnus Ø Arntzen Chloe Piso Carsten Stephan Bernd Thiede Hans-Joachim Mollenkopf Klaus Jung Stefan H E Kaufmann Jörg Schreiber
author_facet	Juan P Patron Annika Fendler Matthias Bild Ulrike Jung Henrik Müller Magnus Ø Arntzen Chloe Piso Carsten Stephan Bernd Thiede Hans-Joachim Mollenkopf Klaus Jung Stefan H E Kaufmann Jörg Schreiber
author_sort	Juan P Patron
title	MiR-133b targets antiapoptotic genes and enhances death receptor-induced apoptosis.
title_short	MiR-133b targets antiapoptotic genes and enhances death receptor-induced apoptosis.
title_full	MiR-133b targets antiapoptotic genes and enhances death receptor-induced apoptosis.
title_fullStr	MiR-133b targets antiapoptotic genes and enhances death receptor-induced apoptosis.
title_full_unstemmed	MiR-133b targets antiapoptotic genes and enhances death receptor-induced apoptosis.
title_sort	mir-133b targets antiapoptotic genes and enhances death receptor-induced apoptosis.
publisher	Public Library of Science (PLoS)
publishDate	2012
url	https://doaj.org/article/68eeae15a69047a5905ae63710d8d6e6
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MiR-133b targets antiapoptotic genes and enhances death receptor-induced apoptosis.

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