WESIERSKA-GADEK, Jozefa, Daniela SCHLOFFER, Vladimír KOTALA and Marcel HORKÝ. Escape of p53 protein from E6-mediated degradation in HeLa cells after cisplatin therapy. International Journal of Cancer. USA: Wiley InterScience, 2002, vol. 101, No 2, p. 128-135. ISSN 0020-7136.
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Basic information
Original name Escape of p53 protein from E6-mediated degradation in HeLa cells after cisplatin therapy
Authors WESIERSKA-GADEK, Jozefa (40 Austria, guarantor), Daniela SCHLOFFER (40 Austria), Vladimír KOTALA (203 Czech Republic) and Marcel HORKÝ (203 Czech Republic).
Edition International Journal of Cancer, USA, Wiley InterScience, 2002, 0020-7136.
Other information
Original language English
Type of outcome Article in a journal
Field of Study Genetics and molecular biology
Country of publisher Czech Republic
Confidentiality degree is not subject to a state or trade secret
Impact factor Impact factor: 4.056
RIV identification code RIV/00216224:14110/02:00007250
Organization unit Faculty of Medicine
UT WoS 000177622600004
Keywords in English apoptosis; nucleolar segregation; E6; cisplatin; PARP-1
Tags apoptosis, cisplatin, E6, nucleolar segregation, PARP-1
Changed by Changed by: Mgr. Vladimír Kotala, Ph.D., učo 68452. Changed: 16/1/2003 16:13.
Abstract
We previously reported that therapy of human cervical carcinoma HeLa cells with CP induced segregation of nucleoli and changes of nuclei characteristic of apoptosis. We raised the question of whether p53 can be reactivated by chemotherapy in HeLa cells despite the presence of HPV-encoded E6 activity. Since the reduced stability of wild-type p53 protein in HeLa cells is a consequence of its enhanced ubiquitination by virally encoded E6 protein, resulting in its accelerated degradation, we checked the cellular level of E6 during CP therapy. Six hours after application of CP, E6 protein expression was markedly reduced. This coincided with the increase of cellular p53 and preceded the nucleolar accumulation of p53 protein, indicating that repression of virally coded E6 protein by CP contributes to the restoration of p53 expression.
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MSM 141100002, plan (intention)Name: Molekulární patofyziologie multigenních chorob
Investor: Ministry of Education, Youth and Sports of the CR, Molecular pathophysiology of multigene diseases
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