Bcl-3 regulates UVB-induced apoptosis

被引：10

作者：

Garcia, Ingrid ^{[1
]}

Cosio, Gabriela ^{[1
]}

Lizarraga, Floria ^{[2
]}

Martinez-Ruiz, Gustavo ^{[2
]}

Melendez-Zajgla, Jorge ^{[2
]}

Ceballos, Gisela ^{[2
]}

Espinosa, Magali ^{[2
]}

Pacheco, Rosario ^{[2
]}

Maldonado, Vilma ^{[2
]}

机构：

[1] Natl Inst Cancerol, Mexico City 14080, DF, Mexico

[2] Natl Inst Genom Med, Mol Biol Lab, Basic Res Div, Mexico City 01900, DF, Mexico

来源：

HUMAN CELL | 2013年 / 26卷 / 02期

关键词：

Bcl-3; Apoptosis; DNA damage; UVB; CANDIDATE PROTOONCOGENE BCL-3; B-CELL LEUKEMIA; FACTOR-KAPPA-B; MITOCHONDRIAL APOPTOSIS; DNA-DAMAGE; CASPASE ACTIVATION; DEATH RECEPTORS; P53; ACTIVATION; BREAST-CANCER; CYTOCHROME-C;

D O I：

10.1007/s13577-012-0056-1

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

B cell leukemia-3 (Bcl-3) has been defined as an anti-apoptotic gene; however, the exact mechanisms through which Bcl-3 influences apoptosis have been elusive. To determine the specific role of Bcl-3 in apoptosis, we evaluated the effect of its silencing on the expression of proteins involved in either the extrinsic or intrinsic apoptotic pathways induced by ultraviolet light B-mediated DNA damage. We found that, in Bcl-3-silenced cells, caspase-3, caspase-8 and caspase-9 activation is accelerated and tBid mitochondrial content is increased. It is important to note that, although mitochondrial Smac levels were reduced after UV exposure, the rate of reduction was slightly higher in Bcl-3 silenced cells than in control cells. Additionally, p53 levels diminished in Bcl-3 silenced cells compared to control cells, as did those of DNA-PK, a DNA repair protein. Altogether, our data indicate that Bcl-3 protects cells from apoptosis by regulating both apoptotic pathways.

引用

页码：47 / 55

页数：9

共 56 条

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