Emerging data on androgen receptor splice variants in prostate cancer

Cao, Subing; Yang, Zhan; Dong, Yan

doi:10.1530/erc-16-0298

Cited by 53 publications

(43 citation statements)

References 118 publications

(196 reference statements)

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“…As such, steroid hormones other than testosterone and DHT may be of great clinical interest considering their suspected involvement in resistance mechanisms. Also, the role of steroidal ligands for activation of (hetero)dimers of various splice variants of the AR constitutes an expanding field of interest (Cao et al 2016).…”

Section: :11mentioning

confidence: 99%

Circulating steroid hormone variations throughout different stages of prostate cancer

Snaterse¹,

Visser²,

Arlt³

et al. 2017

Endocrine-Related Cancer

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Steroid hormones play a central role in the maintenance and progression of prostate cancer. The androgen receptor is the primary driver of tumor cell proliferation and is activated by the androgens testosterone and 5α-dihydrotestosterone. Inhibition of this pathway through medical or surgical castration improves survival in the majority of advanced prostate cancer patients. However, conversion of adrenal androgen precursors and alternative steroidogenic pathways have been found to contribute to tumor progression and resistance to treatment. The emergence of highly accurate detection methods allows us to study steroidogenic mechanisms in more detail, even after treatment with potent steroidogenic inhibitors such as the CYP17A1 inhibitor abiraterone. A clear overview of steroid hormone levels in patients throughout the local, metastatic and castration-resistant stages of prostate cancer and treatment modalities is key toward a better understanding of their role in tumor progression and treatment resistance. In this review,

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Section: :11mentioning

confidence: 99%

Circulating steroid hormone variations throughout different stages of prostate cancer

Snaterse¹,

Visser²,

Arlt³

et al. 2017

Endocrine-Related Cancer

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“…Progression to CRPC is believed to involve reprogramming of the AR transcriptional landscape and a selective pressure for cells to maintain AR activity even in lower concentrations of circulating androgens (Sharma et al 2013, Mills 2014. AR signalling can be maintained through gene amplification (Visakorpi et al 1995), activating mutations (Veldscholte et al 1990, Steinkamp et al 2009), AR splice 24:3 variants (Sun et al 2010, Cao et al 2016 or crosstalk with other oncogenic signalling pathways (Zhu & Kyprianou 2008, Liao et al 2013.…”

Section: Introductionmentioning

confidence: 99%

Glycosylation is a global target for androgen control in prostate cancer cells

Munkley¹

2017

Endocrine-Related Cancer

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Changes in glycan composition are common in cancer and can play important roles in all of the recognised hallmarks of cancer. We recently identified glycosylation as a global target for androgen control in prostate cancer cells and further defined a set of 8 glycosylation enzymes (GALNT7, ST6GalNAc1, GCNT1, UAP1, PGM3, CSGALNACT1, ST6GAL1 and EDEM3), which are also significantly upregulated in prostate cancer tissue. These 8 enzymes are under direct control of the androgen receptor (AR) and are linked to the synthesis of important cancer-associated glycans such as sialyl-Tn (sTn), sialyl LewisX (SLeX), O-GlcNAc and chondroitin sulfate. Glycosylation has a key role in many important biological processes in cancer including cell adhesion, migration, interactions with the cell matrix, immune surveillance, cell signalling and cellular metabolism. Our results suggest that alterations in patterns of glycosylation via androgen control might modify some or all of these processes in prostate cancer. The prostate is an abundant secretor of glycoproteins of all types, and alterations in glycans are, therefore, attractive as potential biomarkers and therapeutic targets. Emerging data on these often overlooked glycan modifications have the potential to improve risk stratification and therapeutic strategies in patients with prostate cancer.

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“…AR activity remains active in CRPC, and increased expression of AR and its splice variants, AR variants (AR-Vs), which lack the ligand-binding domain, is an important mechanism of AR reactivation in CRPC (reviewed in Refs. 1,2 ).…”

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confidence: 99%

Raddeanin A down‐regulates androgen receptor and its splice variants in prostate cancer

Xia

Bai

et al. 2019

J Cellular Molecular Medi

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Castration‐resistant progression of prostate cancer is a major cause of prostate cancer mortality, and increased expression and activity of the full‐length and the splice variants of androgen receptor (AR) have been indicated to drive castration resistance. Consequently, there is an urgent need to develop agents that can target both the full‐length and the splice variants of AR for more effective treatment of prostate cancer. In the present study, we showed that raddeanin A (RA), an oleanane‐type triterpenoid saponin, suppresses the transcriptional activities of both the full‐length and the splice variants of AR. This is attributable to their decreased expression as a result of RA induction of proteasome‐mediated degradation and inhibition of the transcription of the AR gene. We further showed the potential of using RA to enhance the growth inhibitory efficacy of docetaxel, the first‐line chemotherapy for prostate cancer. This study identifies RA as a new agent to target both the full‐length and the splice variants of AR and provides a rationale for further developing RA for prostate cancer treatment.

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Emerging data on androgen receptor splice variants in prostate cancer

Cited by 53 publications

References 118 publications

Circulating steroid hormone variations throughout different stages of prostate cancer

Circulating steroid hormone variations throughout different stages of prostate cancer

Glycosylation is a global target for androgen control in prostate cancer cells

Raddeanin A down‐regulates androgen receptor and its splice variants in prostate cancer

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