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Titolo:
Caspase-mediated Cdk2 activation is a critical step to execute transforming growth factor-beta 1-induced apoptosis in human gastric cancer cells
Autore:
Kim, SG; Kim, SN; Jong, HS; Kim, NK; Hong, SH; Kim, SJ; Bang, YJ;
Indirizzi:
Seoul Natl Univ, Coll Med, Dept Internal Med, Canc Res Inst, Seoul 110744,South Korea Seoul Natl Univ Seoul South Korea 110744 Inst, Seoul 110744,South Korea Seoul Natl Univ, Sch Biol Sci, Seoul 151742, South Korea Seoul Natl Univ Seoul South Korea 151742 Sci, Seoul 151742, South Korea Seoul Natl Univ, Inst Mol Biol & Genet, Seoul 151742, South Korea Seoul Natl Univ Seoul South Korea 151742 enet, Seoul 151742, South Korea Seoul Natl Univ, Coll Med, Dept Internal Med, Seoul 110744, South Korea Seoul Natl Univ Seoul South Korea 110744 Med, Seoul 110744, South Korea NCI, Lab Cell Regulat & Carcinogenesis, Bethesda, MD 20892 USA NCI Bethesda MD USA 20892 egulat & Carcinogenesis, Bethesda, MD 20892 USA
Titolo Testata:
ONCOGENE
fascicolo: 10, volume: 20, anno: 2001,
pagine: 1254 - 1265
SICI:
0950-9232(20010308)20:10<1254:CCAIAC>2.0.ZU;2-N
Fonte:
ISI
Lingua:
ENG
Soggetto:
DEPENDENT PROTEIN-KINASES; FACTOR-BETA; TGF-BETA; CYCLE ARREST; RETINOBLASTOMA PROTEIN; EPITHELIAL-CELLS; THYMOCYTE APOPTOSIS; HEPATOMA-CELLS; INHIBITION; DEATH;
Keywords:
TGF-beta 1; apoptosis; caspase-3; cyclin-dependent kinase-2; p21(cip1); p27(kip1);
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
45
Recensione:
Indirizzi per estratti:
Indirizzo: Bang, YJ Seoul Natl Univ, Coll Med, Dept Internal Med, Canc Res Inst, 28 Yongon Dong, Seoul 110744, South Korea Seoul Natl Univ 28 Yongon Dong SeoulSouth Korea 110744 th Korea
Citazione:
S.G. Kim et al., "Caspase-mediated Cdk2 activation is a critical step to execute transforming growth factor-beta 1-induced apoptosis in human gastric cancer cells", ONCOGENE, 20(10), 2001, pp. 1254-1265

Abstract

Although TGF-beta1, a growth inhibitor, is known to also induce apoptosis,the molecular mechanism of this apoptosis is largely undefined, Here, we identify the mechanism of TGF-beta1-induced apoptosis in SNU-16 human gastric cancer cells. Cell cycle and TUNEL analysis showed that, upon TGF-beta1 treatment, cells mere initially arrested at the G1 phase and then driven into apoptosis, Of note, caspase-3 was activated in accordance with TGF-beta1-induced G1 arrest, Activated caspase-3 is targeted to cleave p21(cip1), p27(kip1), and Rb, which play important roles in TGF-beta -induced G1 arrest, into;inactive fragments. Subsequently, Cdk2 was aberrantly activated due tothe cleavage of p21 and p27, We found that the inhibition of Cdk2 activityefficiently blocks TGF-beta1-induced apoptosis, whereas it did; not prevent caspase-3 activation or the subsequent cleavage of target proteins, In contrast, the suppression of caspase-3 activity inhibited the cleavage of target proteins, the activation of Cdk2, and the induction of apoptosis. Takentogether, our results suggest that activation of caspase-3 by TGF-beta1 may initiate the conversion from G1 cell cycle arrest to apoptosis via the cleavage of p21, p27 and Rb, which in turn causes Cdk2 activation and, most significantly, Cdk2 activation as a downstream effector of caspase is a critical step for the execution TGF-beta1-induced apoptosis.

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Documento generato il 04/07/20 alle ore 20:26:19