Abstract
A major challenge in clinical management of prostate cancer (PC) is to limit tumor growth and prevent metastatic spreading. Considerable efforts have been made to discover new compounds for PC therapy and recent years have seen promising progress in this field. Pharmacological approaches have been designed to achieve benefits in PC treatment and avoid the negative side effects resulting from administration of antagonists or agonists or new drugs. Nonetheless, the currently available therapies frequently induce resistance and PC progresses toward castration-resistant forms that can be caused by the androgen receptor reactivation and/or mutations, or derangement of signaling pathways. Preclinical and clinical findings have also shown that other nuclear receptors are frequently altered in PC. In this review, we focus on the role of estradiol/estradiol receptor (ER) axis, which controls PC growth and progression. Selective targeting of ER subtypes (α or β) may be an attractive way to limit the growth and spreading of prostatic cancer cells.
Highlights
Prostate cancer (PC) is one of the most frequently diagnosed cancers and a leading cause of cancerrelated deaths in Europe, with around 417,000 new cases diagnosed in 2012
Estrogen levels increase in men during inflammatory processes and obesity [25]. This hormonal fluctuation might explain the relationship between inflammation, obesity, and prostate cancer (PC) frequently observed in elderly men
estrogen receptor α (ERα) is mainly expressed in stromal cells within the non-malignant human prostate, though is occasionally found in basal-epithelial cells, whereas ERβ is mainly confined to basal-epithelial cells [33,34,35]
Summary
A major challenge in clinical management of prostate cancer (PC) is to limit tumor growth and prevent metastatic spreading. Considerable efforts have been made to discover new compounds for PC therapy and recent years have seen promising progress in this field. The currently available therapies frequently induce resistance and PC progresses toward castration-resistant forms that can be caused by the androgen receptor reactivation and/or mutations, or derangement of signaling pathways. Preclinical and clinical findings have shown that other nuclear receptors are frequently altered in PC. We focus on the role of estradiol/estradiol receptor (ER) axis, which controls PC growth and progression. Selective targeting of ER subtypes (α or β) may be an attractive way to limit the growth and spreading of prostatic cancer cells
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