AKT1/BRCA1 in the control of homologous recombination and genetic stability: the missing link between hereditary and sporadic breast cancers
2010
AKT1 and BRCA1: Links in Breast Cancer
publication
Evidence: moderate
Author Information
Author(s): Guirouilh-Barbat Josée, Wilhelm Therese, Lopez Bernard S.
Primary Institution: CNRS, UMR217, Institut de radiobiologie cellulaire et moléculaire, France
Hypothesis
Does the activation of AKT1 in sporadic breast cancers lead to a phenotype similar to that observed in familial cancers?
Conclusion
The study suggests that the over-activation of AKT1 in sporadic breast cancers may mimic the BRCA1-deficient phenotype, linking sporadic and hereditary breast cancers.
Supporting Evidence
- AKT1 is upregulated in about 50% of sporadic breast cancers.
- BRCA1 is essential for homologous recombination, a process crucial for maintaining genome stability.
- Overexpression of AKT1 leads to the cytoplasmic retention of BRCA1 and RAD51, inhibiting their nuclear functions.
Takeaway
This study looks at how a protein called AKT1 might cause breast cancer by affecting another protein called BRCA1, which helps fix DNA. If AKT1 is too active, it can lead to problems that make cells more likely to become cancerous.
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