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Titolo:
Ras-mediated suppression of TGF beta RII expression in intestinal epithelial cells involves Raf-independent signaling
Autore:
Bulus, NM; Sheng, HM; Sizemore, N; Oldham, SM; Barnett, JV; Coffey, RJ; Beauchamp, DR; Barnard, JA;
Indirizzi:
Vanderbilt Univ, Sch Med, Dept Pediat, Nashville, TN 37232 USA Vanderbilt Univ Nashville TN USA 37232 pt Pediat, Nashville, TN 37232 USA Vanderbilt Univ, Sch Med, Dept Surg, Nashville, TN 37232 USA Vanderbilt Univ Nashville TN USA 37232 Dept Surg, Nashville, TN 37232 USA Vanderbilt Univ, Sch Med, Dept Med, Nashville, TN 37232 USA Vanderbilt Univ Nashville TN USA 37232 Dept Med, Nashville, TN 37232 USA Vanderbilt Univ, Sch Med, Dept Cell Biol, Nashville, TN 37232 USA Vanderbilt Univ Nashville TN USA 37232 Cell Biol, Nashville, TN 37232 USA Vanderbilt Univ, Sch Med, Vanderbilt Canc Ctr, Nashville, TN 37232 USA Vanderbilt Univ Nashville TN USA 37232 Canc Ctr, Nashville, TN 37232 USA Univ Zurich, Inst Zool, Zurich, Switzerland Univ Zurich Zurich Switzerland v Zurich, Inst Zool, Zurich, Switzerland
Titolo Testata:
NEOPLASIA
fascicolo: 4, volume: 2, anno: 2000,
pagine: 357 - 364
SICI:
1522-8002(200007/08)2:4<357:RSOTBR>2.0.ZU;2-C
Fonte:
ISI
Lingua:
ENG
Soggetto:
GROWTH-FACTOR-BETA; HUMAN COLORECTAL CANCERS; RHO-FAMILY PROTEINS; II RECEPTOR GENE; MICROSATELLITE INSTABILITY; MUTATION ANALYSIS; ONCOGENIC RAS; CYCLIN D1; IN-VIVO; HA-RAS;
Keywords:
Ras; colorectal carcinoma; TGF beta; Raf; intestinal epithelium; TGF beta RII;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
62
Recensione:
Indirizzi per estratti:
Indirizzo: Barnard, JA 700 Childrens Dr, Columbus, OH 43205 USA 700 Childrens Dr Columbus OH USA 43205 Columbus, OH 43205 USA
Citazione:
N.M. Bulus et al., "Ras-mediated suppression of TGF beta RII expression in intestinal epithelial cells involves Raf-independent signaling", NEOPLASIA, 2(4), 2000, pp. 357-364

Abstract

Ras-transformed intestinal epithelial cells are resistant to the growth inhibitory actions of TGF beta and have a marked decrease in expression of the TGF beta type II receptor (TGF beta RII). Rat intestinal epithelial cells(RIE) were stably transfected with activated Ras, Sos and Raf constructs and tested for expression of TGF beta RII and sensitivity to growth inhibition by TGF beta. The parental RIE line and the RIE-Raf cells were nontransformed in morphology and were sensitive to TGF beta (70-90% inhibited). In contrast, the RIE-Ras and RIB-sos lines were transformed, resistant to TGF beta and expressed 5- to 10-fold decreased levels of the TGF beta RII mRNA and protein. Cyclin D1 protein expression was repressed by TGF beta treatmentin parental RIE and RIE-Raf cells, whereas levels of cyclin D1 in RIE-Ras and RIB-sos cells remained unchanged. Treatment of RIE-Ras cells with 25 muM farnesyl transferase inhibitor, FTI L739,749, for 48 hours restored expression of TGF beta RII to levels equivalent to control cells. In addition, treatment of RIE-Ras cells for 48 hours with PD-98059, a specific MAPKK inhibitor, also increased expression of TGF beta RII to control levels. Collectively these results suggest that downregulation of TGF beta RII and loss of sensitivity to growth inhibition by TGF beta in Ras-transformed intestinal epithelial cells is not mediated exclusively by the conventional Ras/Raf/MAPKK/MAPK pathway. However, activation of MAPK, perhaps by an alternate Ras effector pathway, appears to be necessary for Ras-mediated downregulationof TGF beta RII.

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Documento generato il 04/07/20 alle ore 18:03:36