Open AccessMolecular mechanisms regulating the hormone sensitivity of breast cancer
Author(s) -
Tokunaga Eriko,
Hisamatsu Yuichi,
Tanaka Kimihiro,
Yamashita Nami,
Saeki Hiroshi,
Oki Eiji,
Kitao Hiroyuki,
Maehara Yoshihiko
Publication year - 2014
Publication title -
cancer science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.035
H-Index - 141
eISSN - 1349-7006
pISSN - 1347-9032
DOI - 10.1111/cas.12521
Subject(s) - pi3k/akt/mtor pathway , breast cancer , foxa1 , estrogen receptor , cancer research , protein kinase b , endocrine system , medicine , hormone , cancer , biology , endocrinology , signal transduction , microbiology and biotechnology
Breast cancer is a heterogeneous disease. Approximately 70% of breast cancers are estrogen receptor ( ER ) positive. Endocrine therapy has dramatically improved the prognosis of ER ‐positive breast cancer; however, many tumors exhibit de novo or acquired resistance to endocrine therapy. A thorough understanding of the molecular mechanisms regulating hormone sensitivity or resistance is important to improve the efficacy of and overcome the resistance to endocrine therapy. The growth factor receptor signaling pathways, particularly the phosphatidylinositol 3‐kinase (PI3K)/Akt/mammalian target of rapamycin ( mTOR ) pathway can mediate resistance to all forms of endocrine therapy. In contrast, FOXA 1 transcription factor is a key determinant of ER function and endocrine response. Intriguingly, a link between hormone resistance induced by the PI3K/Akt/ mTOR pathway and the function of FOXA 1 has been suggested. In this review, we focus on the PI3K/Akt/ mTOR pathway and functions of FOXA 1 in terms of the molecular mechanisms regulating the hormone sensitivity of breast cancer.