Functional disruption of IEX-1 expression by concatemeric hammerhead ribozymes alters growth properties of 293 cells

FEBS Letters
O GrobeH Schäfer

Abstract

The early response gene IEX-1 modulates apoptosis and cell growth in a poorly defined fashion. Here, we describe the effect of hammerhead ribozymes specifically disrupting IEX-1 expression in 293 cells. Compared to vector control, 293 cells exhibit a reduced growth rate and a slowed cell cycle progression, when stably transfected with a concatemeric ribozyme construct. In addition, these 293 cells were much less sensitive to apoptosis induced by an activating Fas/CD95 antibody or by the anti-cancer drugs etoposide and doxorubicin. By modulating the cell cycle, IEX-1 might be part of a growth signal if favourable growth conditions prevail, whereas under unfavourable conditions, i.e. death receptor activation, IEX-1 facilitates apoptosis.

References

Oct 1, 1992·Experimental Cell Research·K Brasch, R L Ochs
Feb 27, 1998·Frontiers in Bioscience : a Journal and Virtual Library·B AmatiJ Vlach
Mar 21, 1998·Science·Z G WangP P Pandolfi
May 20, 1998·Biochemical and Biophysical Research Communications·A PietzschG Schmitz
Aug 28, 1998·Science·G Evan, T Littlewood
Oct 29, 1998·Biochemical and Biophysical Research Communications·T KobayashiR Kumar
Jan 8, 1999·Biochemical and Biophysical Research Communications·R KumarM R Pittelkow
Aug 10, 1999·BioEssays : News and Reviews in Molecular, Cellular and Developmental Biology·M V Blagosklonny
Aug 17, 1999·Biochemical and Biophysical Research Communications·H SchäferW E Schmidt
Dec 22, 1999·Current Opinion in Cell Biology·M Guo, B A Hay
Jun 30, 2000·The Journal of Biological Chemistry·D L SegevS Maheswaran
Nov 18, 2000·The EMBO Journal·V FogalG Del Sal

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Citations

Jun 20, 2008·Neuropathology : Official Journal of the Japanese Society of Neuropathology·Kentaro YamashitaToru Iwama
Feb 18, 2009·Retrovirology·Zachary KlaseFatah Kashanchi
Nov 21, 2007·Annals of Surgical Oncology·Tetsuro SasadaArimichi Takabayashi
Jan 10, 2002·Proceedings of the National Academy of Sciences of the United States of America·Y ZhangMei X Wu
Jan 29, 2005·Proceedings of the National Academy of Sciences of the United States of America·Paul LabhartCarolyn L Smith
Nov 30, 2010·European Journal of Cell Biology·Alexander Arlt, Heiner Schäfer
Sep 9, 2006·Journal of Cellular Biochemistry·Fukka YouShigeru Nakashima
Sep 29, 2004·Biochemical and Biophysical Research Communications·Rajiv KumarHee-Jeong Im
Nov 17, 2011·Ultrastructural Pathology·Liping HanMei X Wu
May 4, 2004·The Journal of Steroid Biochemistry and Molecular Biology·Abdelhabib SemlaliMarie-Josèphe Duchesne
Oct 10, 2003·Oncogene·Yujin ZhangMei X Wu
Oct 31, 2018·Journal of the American Heart Association·Mohd ShahidMei X Wu
Mar 29, 2006·The Journal of Biological Chemistry·Li ShenMei X Wu
Feb 15, 2002·The Journal of Biological Chemistry·Hee-Jeong ImRajiv Kumar
Dec 8, 2017·Oxidative Medicine and Cellular Longevity·Ming-Jiang XuXian Wang
Apr 19, 2003·The Journal of Immunology : Official Journal of the American Association of Immunologists·Yosuke OsawaShigeru Nakashima
Sep 17, 2005·Journal of Applied Physiology·Stacy L SommerRajiv Kumar

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Apoptosis

Apoptosis is a specific process that leads to programmed cell death through the activation of an evolutionary conserved intracellular pathway leading to pathognomic cellular changes distinct from cellular necrosis