Abstract
Despite androgen dependence in a majority of castration-resistant prostate cancers, some cancer cells are independent of androgen receptor (AR) function, a feature of heterogeneity in prostate cancer. One of the aggressive variants of prostate cancer that are AR independent is neuroendocrine prostate cancer (NEPC). This manuscript will focus on the new finding of human one cut domain family member 2 (ONECUT2) transcription factor and its role in castration resistance, especially in NEPC.
Highlights
Prostate cancer is the most common cancer diagnosed in men and the second leading cause of cancerrelated deaths in the United States[1]
Given its dependence on the androgen receptor (AR) axis, prostate adenocarcinoma can respond to androgen deprivation therapy (ADT) for a variable duration, but eventually, it progresses to www.cdrjournal.com
Recent studies spearheaded by Rotinen et al.[5] and Guo et al.[6] showed that one cut domain family member 2 (ONECUT2) is an important regulator of AR-mediated growth and a driver of NE differentiation in transition from adenocarcinoma to neuroendocrine prostate cancer (NEPC), and is being investigated as a new drug target with potential therapeutic implications
Summary
Prostate cancer is the most common cancer diagnosed in men and the second leading cause of cancerrelated deaths in the United States[1]. In contrast to ONECUT1, ONECUT2 expression has been shown to be elevated in multiple different cancers, including prostate cancer[6], ovarian cancer[9], gastric cancer[10], colorectal cancer[11], hepatocellular carcinoma[12], lung adenocarcinoma[13], and neuroendocrine tumors[6]. ONECUT2 target genes are involved in the cell cycle, angiogenesis, and hypoxia, which in turn are implicated in tumor growth and metastasis in prostate cancer[6].
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