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Gene Review:

BRCC3 - BRCA1/BRCA2-containing complex, subunit 3

Homo sapiens

Synonyms: BRCA1-A complex subunit BRCC36, BRCA1/BRCA2-containing complex subunit 3, BRCA1/BRCA2-containing complex subunit 36, BRCC36, BRISC complex subunit BRCC36, ...

Boudreau, H.E. et al., Chen, X. et al., Dong, Y. et al., Brinke, A. et al.

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Disease relevance of BRCC3

BRCC36 shows aberrant expression in sporadic breast tumors [1].

High impact information on BRCC3

BRCC36 and BRCC45 are novel components of the complex with sequence homology to a subunit of the signalosome and proteasome complexes [1].
Furthermore, exons located beyond the known C6.1A sequence and present in normal transcripts precede exons 2-26 of the factor VIII gene in the hybrid mRNA of the haemophilic twins [2].
Importantly, BRCC36 depletion disrupts IR-induced phosphorylation of BRCA1 [3].
Knock-down of BRCC36 alone does not affect cell growth, but when combined with ionizing radiation (IR) exposure, it leads to an increase in the percentage of cells undergoing apoptosis when compared with the small interfering RNA control group in breast cancer cells [3].
These results show that down-regulation of BRCC36 expression impairs the DNA repair pathway activated in response to IR by inhibiting BRCA1 activation, thereby sensitizing breast cancer cells to IR-induced apoptosis [3].

Biological context of BRCC3

Furthermore, exogenous BRCC3 expression was associated with a delay in etoposide-induced cell death and an increase in cell proliferation [4].
Expression levels of BRCC3 mRNA and protein are high during G2/M phase of the cell cycle in breast cancer cells [4].
BRCC3 is localized at human chromosome 5q12 [4].
1. BRCC3 open reading frame consists of 529 amino acids, coding for an approximate 60-kDa predominantly membrane-associated protein [4].
These findings demonstrate that BRCC3 is a novel effector of Raf-1, and implicate a role of BRCC3 in modulation of p-ERK, cell survival and proliferation [4].

Anatomical context of BRCC3

Transient or stable expression of the epitope-tagged BRCC3 cDNA was associated with increased p-ERK in three different cell lines [4].

Other interactions of BRCC3

Immunofluorescent staining of BRCA1 and gamma-H2AX indicates that BRCC36 depletion prevents the formation of BRCA1 nuclear foci in response to DNA damage in breast cancer cells [3].
Expression of BRCC3, a novel cell cycle regulated molecule, is associated with increased phospho-ERK and cell proliferation [4].

References

Regulation of BRCC, a holoenzyme complex containing BRCA1 and BRCA2, by a signalosome-like subunit and its role in DNA repair. Dong, Y., Hakimi, M.A., Chen, X., Kumaraswamy, E., Cooch, N.S., Godwin, A.K., Shiekhattar, R. Mol. Cell (2003) [Pubmed]
Two chimaeric transcription units result from an inversion breaking intron 1 of the factor VIII gene and a region reportedly affected by reciprocal translocations in T-cell leukaemia. Brinke, A., Tagliavacca, L., Naylor, J., Green, P., Giangrande, P., Giannelli, F. Hum. Mol. Genet. (1996) [Pubmed]
BRCC36 is essential for ionizing radiation-induced BRCA1 phosphorylation and nuclear foci formation. Chen, X., Arciero, C.A., Wang, C., Broccoli, D., Godwin, A.K. Cancer Res. (2006) [Pubmed]
Expression of BRCC3, a novel cell cycle regulated molecule, is associated with increased phospho-ERK and cell proliferation. Boudreau, H.E., Broustas, C.G., Gokhale, P.C., Kumar, D., Mewani, R.R., Rone, J.D., Haddad, B.R., Kasid, U. Int. J. Mol. Med. (2007) [Pubmed]

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