J 2015

Overexpression of the Delta Np73 isoform is associated with centrosome amplification in brain tumor cell lines

MIKULENKOVÁ, Erika, Jakub NERADIL, Karel ZITTERBART, Jaroslav ŠTĚRBA, Renata VESELSKÁ et. al.

Basic information

Original name

Overexpression of the Delta Np73 isoform is associated with centrosome amplification in brain tumor cell lines

Authors

MIKULENKOVÁ, Erika (203 Czech Republic, belonging to the institution), Jakub NERADIL (203 Czech Republic, belonging to the institution), Karel ZITTERBART (203 Czech Republic, belonging to the institution), Jaroslav ŠTĚRBA (203 Czech Republic, belonging to the institution) and Renata VESELSKÁ (203 Czech Republic, guarantor, belonging to the institution)

Edition

Tumor Biology, Dordrecht, Springer, 2015, 1010-4283

Other information

Language

English

Type of outcome

Článek v odborném periodiku

Field of Study

30200 3.2 Clinical medicine

Country of publisher

Netherlands

Confidentiality degree

není předmětem státního či obchodního tajemství

Impact factor

Impact factor: 2.926

RIV identification code

RIV/00216224:14310/15:00084860

Organization unit

Faculty of Science

UT WoS

000362969900018

Keywords in English

centrosome amplification; medulloblastoma; glioblastoma multiforme; Delta Np73; TAp73; BubR1

Tags

Tags

International impact, Reviewed
Změněno: 24/5/2017 17:02, Ing. Nicole Zrilić

Abstract

V originále

The p73 protein is a member of the p53 family, and this protein is known to be essential for the maintenance of genomic stability, DNA repair, and apoptosis regulation. Transcription from two promoters leads to two main N-terminal isoforms: the TAp73 isoform is reported to have tumor suppressor function, whereas the DeltaNp73 isoform likely has oncogenic potential. The present study is focused on the investigation of a possible role of both these p73 N-terminal isoforms in the process of centrosome amplification. HGG-02 and GM7 glioblastoma cell lines and the Daoy medulloblastoma cell line were used in this study. The cells were analyzed using indirect immunofluorescence to determine TAp73 and DeltaNp73 expression patterns and possible co-localization with the BubR1 protein, as well as the number of centrosomes. A transiently transfected GM7 cell line was used to verify the results concerning the N-terminal isoforms in relation to centrosome amplification. We found that increased immunoreactivity for the DeltaNp73 isoform is associated with the occurrence of an abnormal number of centrosomes in particular cells. Using the transiently transfected GM7 cell line, we confirmed that centrosome amplification is present in cells with overexpression of the DeltaNp73 isoform. In contrast, the immunoreactivity for the TAp73 isoform was weak or medium in most of the cells with an aberrant number of centrosomes. To determine the putative counterpart of the p73 N-terminal isoforms among spindle assembly checkpoint (SAC) proteins, we also evaluated possible interactions between the N-terminal isoforms and BubR1 protein, but no co-localization of these proteins was observed.

Links

EE2.3.20.0183, research and development project
Name: Centrum experimentální biomedicíny
MUNI/C/0804/2011, interní kód MU
Name: Exprese N-terminálních izoforem proteinu p73 ve vztahu k aberacím centrosomů v nádorových buňkách.
Investor: Masaryk University, Rector's Program