Androgen receptor (AR) is closely associated with the occurrence and progression of breast cancer; however, the clinical significance of it in triple negative breast cancer (TNBC) has been controversial.
In survival analysis, a higher level of AR expression correlated with prolonged overall survival in metastatic BC (high expression vs. low expression, median OS 53.1 vs. 27.2 months, p=.001).
Our data suggested that AR/let-7a signaling could inhibit the biological behavior of tumor-initiating cells (T-IC) in ER+AR+ breast cancers, which might become a new therapeutic target.
Application to 213 phenotypes and 1,544 TF binding datasets identified 2,264 relationships between hundreds of TFs and 94 phenotypes, including androgen receptor in prostate cancer and GATA3 in breast cancer.
In this review, we aim to address the importance of the AR in BCa diagnosis and prognosis, current AR-targeting approaches in BCa, and the potential for AR-downstream molecules to serve as therapeutic targets.
Biochemical inhibition of STAT3 with the small-molecule inhibitor galiellalactone significantly reduced AR activity in several prostate and breast cancer cell lines.
Targeted proteins, associated with different signal transduction pathways, have included transforming growth factor-alpha [TGF-alpha (MR(1))], its binding site the epidermal growth factor receptor [EGFR (MR(2))] sharing sequence homology to the breast cancer prognostic marker Her-2/neu, an apoptosis inhibiting protein [bcl-2 (MR(4))], and the androgen receptor [AR (MR(5))].
The TP53 gene is involved in breast cancer development in the Li-Fraumeni syndrome and Li-Fraumeni syndrom-like families, whereas germ-line mutations in the androgen receptor (AR) gene is present in a subset of male breast cancers.
Long term treatment with therapies aimed at blocking the estrogen- (ER) or androgen receptor (AR) action often leads to the development of resistance to selective modulators of the estrogen receptor (SERMs) in ERα-positive breast cancer, or of the androgen receptor (SARMs) in AR-positive prostate cancer.
For the first time, to the best of our knowledge, we demonstrated that C. comatus and G. lucidum decreased androgen and glucocorticoide receptors transcriptional activity in breast cancer MDA-kb2 cells in a dose-dependent manner, and suppressed androgen receptor (AR) protein level in LNCaP and MDA-kb2 cells.
To elucidate the possible role of genetic variation in the estrogen receptors alpha and beta (ER-alpha, ER-beta) and androgen receptor (AR) genes in breast cancer risk, the -1174(TA)n, c.1092+3607(CA)(n) and c.172(CAG)n repeat polymorphisms of the three genes were studied.
We have investigated the potential link between three tandem repeats (CAG, TA, and CA) in the AR, ERs alpha and beta genes, respectively, and breast cancer.
No cell death was found in the AR-null prostate cancer cell PC-3 or its subline that has been reconstituted with an exogenous AR gene, as well as two breast cancer cell lines that are AR positive.
In AR negative breast tumours, mutation screening identified the same mutation (T105A) in the 5'UTR of two AR negative breast cancer patients but not reported in the normal human population.
In this review, we will discuss some basic aspects of sumoylation and how sumoylation modulates the NR-mediated gene expression, focusing on androgen receptor (AR) and estrogen receptor (ER), a key player in progression of prostate or breast cancer.
In summary, MDA-MB-453 cells express high levels of functional AR, and thus provide a valuable in vitro model for further studies on androgen regulation of gene expression, and perhaps cell proliferation in breast cancer.
Successful treatment with anti-androgen therapy in other androgen receptor-positive malignancies such as prostate and breast cancer has inspired researchers to investigate this treatment in salivary gland cancer as well.