Abstract
Genomic instability finally induces cell death or apoptosis. The tumor suppressor, phosphatase and tensin homolog on chromosome 10 (PTEN), is a dual-specificity phosphatase, which has protein phosphatase activity and lipid phosphatase activity that antagonizes PI3K activity. Cells that lack PTEN have constitutively higher levels of PIP3 and activated downstream PI3K/AKT targets. BRCA1, a well-known breast cancer tumor suppressor, is to associate with breast cancer risk and genetic susceptibility. Many studies have demonstrated that PTEN, as well as BRCA1, plays a critical role in DNA damage responses. The BRCA1 functionally cooperates with PTEN and might be an essential blockage in the development of several tumors. Actually, the PTEN and BRCA1 genes are recognized as one of the most frequently deleted and/or mutated in many human cancers. The PI3K/AKT pathway is constitutively active in BRCA1-defective human cancer cells. Loss or decrease of these PTEN or BRCA1 function, by either mutation or reduced expression, has a role in various tumor developments. This review summarizes recent findings of the function of BRCA1 and PTEN involved in genomic stability and cancer cell signaling.
Highlights
Germline mutations in the breast cancer susceptibility gene 1 (BRCA1) extensively increase the risk of breast and ovarian cancers [1, 2]
This review summarizes recent findings of the function of BRCA1 and Phosphatase and tensin homolog on chromosome 10 (PTEN) involved in genomic stability and cancer cell signaling
BRCA1-related tumorigenesis may be mainly caused by increased DNA damage and decreased genome stability that is a major hallmark of cancer [3]
Summary
Germline mutations in the breast cancer susceptibility gene 1 (BRCA1) extensively increase the risk of breast and ovarian cancers [1, 2]. The PI3K/AKT pathway is constitutively active in BRCA1-defective human cancer cells. Loss or decrease of these PTEN or BRCA1 function, by either mutation or reduced expression, has a role in various tumor developments.
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