Multivariable Cox proportional hazard models were used to assess the association of <i>PTEN/ERG</i> status with lethal prostate cancer (defined as metastasis or prostate cancer specific death), adjusting for patient age, race, pathological grade and stage, and surgical margin status.
We used multivariable Cox regression to examine associations between statins and prostate cancer risk overall, by measures of clinically-significant disease, and by ERG and PTEN status.
We performed integrative analysis for 3 sets of prostate cancer (PCa) genomic data, and found that BMI1 and androgen receptor (AR) were positively correlated, suggesting that AR might regulate BMI1.
Both hormone-sensitive and castration- and enzalutamide-resistant prostate cancers (PCa) depend on the ternary complex factor (TCF) protein ELK1 to serve as a tethering protein for the androgen receptor (AR) to activate a critical set of growth genes.
The major topic areas discussed at this year's meeting included (a) new insights into prostate cancer biology and treatment; (b) approaches for accelerating precision medicine for prostate cancer; (c) prostate-specific membrane antigen-targeted therapy and imaging for prostate cancer; (d) updates on Poly (ADP-ribose) polymerase (PARP)-inhibitor clinical trial results; (e) the biology and role of prostate cancer stem cells; (f) new approaches for targeting the androgen receptor and other steroid hormone receptor pathways; (g) racial disparities in prostate cancer treatment and outcomes; (h) the role of the nervous system in prostate cancer development and progression; (i) the role of the WNT signaling pathway in normal prostate and prostate cancer biology; (j) novel immunotherapy approaches; and (k) the ecology of prostate cancer.
ARD-69 is capable of reducing the AR protein level by >95% in these prostate cancer cell lines and effectively suppressing AR-regulated gene expression.
Despite the AR being one of the most studied and attended targets in cancer, those gain-of-function mutations in the receptor remain a significant challenge for the development of PCa therapies.
In this study, we reported that KDM5C was highly expressed in PCa and CRPC specimens, and the high expression promoted CRPC cell proliferation through repressing phosphatase and tensin homolog (PTEN) gene epigenetically.
Many genes exhibit evidence for allele-specific transcriptional activation by PrCa master-regulators (including androgen receptor) in Position Weight Matrix, Chip-Seq, and Hi-C experimental data, suggesting common regulatory mechanisms for the associated genes.
<b>Conclusions:</b> Our results reveal a previously unidentified cooperative role of RUNX2 overexpression and PTEN haploinsufficiency in prostate tumorigenesis, suggesting that the defined RUNX2-CXCR7-AKT axis can be a viable target for effective treatment of PCa.
Collectively, this work provides a potential lead compound for anticancer agent development related to prostate cancer therapy, and took a step forward towards the development of novel and improved AR antagonists.