Abstract
Triple-negative breast cancer (TNBC) is an aggressive subgroup of human breast cancer, which is characterized as estrogen receptor (ER) negative, progesterone receptor (PR) negative, and human epidermal growth factor receptor 2 (HER2) negative. TNBC is the most difficult breast cancer subgroup to treat, due to its unresponsiveness to current clinical targeted therapies, high rate of recurrence, and poor prognosis. Thus, there is an urgent medical need to identify therapeutic targets and develop more effective stratified medicine for the treatment of TNBC. Here we review the potential therapeutic targets for TNBC based on its intrinsic subtype. We also review the aberrant activated signals found in different subgroups of TNBC, including androgen receptor (AR) and PI3K/AKT/mTOR, Notch, Wnt/β-catenin, Hedge-hog, and TGF-β signaling pathways, which play essential roles in multiple development stages of TNBC. The careful analysis of these signaling pathways and therapeutic targets would have significant impact on the drug development and clinical trials, leading to effective therapies for this deadly disease.
Highlights
Triple-negative breast cancer (TNBC) accounts for approximately 15%–20% of newly diagnosed breast cancer worldwide and occurs more prevalently in Hispanics, American and African women [1,2,3]
Triple-negative breast cancer (TNBC) is an aggressive subgroup of human breast cancer, which is characterized as estrogen receptor (ER) negative, progesterone receptor (PR) negative, and human epidermal growth factor receptor 2 (HER2) negative
We review the aberrant activated signals found in different subgroups of TNBC, including androgen receptor (AR) and PI3K/AKT/mTOR, Notch, Wnt/β-catenin, Hedge-hog, and TGF-β signaling pathways, which play essential roles in multiple development stages of TNBC
Summary
Triple-negative breast cancer (TNBC) accounts for approximately 15%–20% of newly diagnosed breast cancer worldwide and occurs more prevalently in Hispanics, American and African women [1,2,3]. Other PARP inhibitors (Veliparib and Talazoparib) are still under investigation in the cases of BRCA mutation-associated breast cancer The TGF-β, Notch, Wnt/β-catenin signaling pathways and tyrosine-kinase receptors [9, 36, 37] that regulate EMT and CSCs function are abnormally regulated in TNBC.
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