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ErbB-2 nuclear function in breast cancer growth, metastasis and resistance to therapy.
- Source :
-
Endocrine-related cancer [Endocr Relat Cancer] 2016 Dec; Vol. 23 (12), pp. T243-T257. Date of Electronic Publication: 2016 Oct 07. - Publication Year :
- 2016
-
Abstract
- Approximately 15-20% of breast cancers (BC) show either membrane overexpression of ErbB-2 (MErbB-2), a member of the ErbBs family of receptor tyrosine kinases, or ERBB2 gene amplification. Until the development of MErbB-2-targeted therapies, this BC subtype, called ErbB-2-positive, was associated with increased metastatic potential and poor prognosis. Although these therapies have significantly improved overall survival and cure rates, resistance to available drugs is still a major clinical issue. In its classical mechanism, MErbB-2 activates downstream signaling cascades, which transduce its effects in BC. The fact that ErbB-2 is also present in the nucleus of BC cells was discovered over twenty years ago. Also, compelling evidence revealed a non-canonical function of nuclear ErbB-2 as a transcriptional regulator. As a deeper understanding of nuclear ErbB-2 actions would be crucial to the disclosure of its role as a biomarker and a target of therapy in BC, we will here review its function in BC, in particular, its role in growth, metastatic spreading and response to currently available MErbB-2-positive BC therapies.<br /> (© 2016 Society for Endocrinology.)
- Subjects :
- Animals
Antineoplastic Agents therapeutic use
Breast Neoplasms drug therapy
Breast Neoplasms genetics
Female
Gene Expression Regulation, Neoplastic
Humans
Neoplasm Metastasis
Receptor, ErbB-2 genetics
Signal Transduction genetics
Breast Neoplasms pathology
Drug Resistance, Neoplasm genetics
Receptor, ErbB-2 physiology
Subjects
Details
- Language :
- English
- ISSN :
- 1479-6821
- Volume :
- 23
- Issue :
- 12
- Database :
- MEDLINE
- Journal :
- Endocrine-related cancer
- Publication Type :
- Academic Journal
- Accession number :
- 27765799
- Full Text :
- https://doi.org/10.1530/ERC-16-0360