ONECUT2 as a key mediator of androgen receptor-independent cell growth and neuroendocrine differentiation in castration-resistant prostate cancer

Choi, WonSeok; Boland, Julia L.; Lin, Jianqing

doi:10.20517/cdr.2021.108

Cited by 3 publications

(4 citation statements)

References 16 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Moreover, GW4869 treatment significantly inhibited the survival of PTX-resistant prostate cancer cells in a dose-dependent manner and reduced the tumor weight in an in vivo model. Kushwaha et al (2022) performed a critical review and demonstrated the role of prostate cancer stem-like cells (PCSCs) in the development of antiandrogen resistance [8] . PCSCs have the ability to differentiate, selfrenew, and regenerate tumor heterogeneity.…”

Section: Article Descriptionmentioning

confidence: 99%

“…The methods for isolation, identification, and characterization of PCSCs from primary prostate tumors have also been described. Choi et al (2022) provided a perspective on the transcription factor ONECUT2 which mediates ARindependent cell growth and neuroendocrine differentiation in CRPC [9] . It is a key factor in NE differentiation between adenocarcinoma to neuroendocrine prostate cancer (NEPC).…”

Section: Article Descriptionmentioning

confidence: 99%

See 1 more Smart Citation

New insights for drug resistance in metastatic castration-resistant prostate cancer

Kushwaha¹,

Gupta²

2022

Cancer Drug Resist

View full text Add to dashboard Cite

Prostate cancer is the most common cancer and is the second leading cause of cancer-related deaths among men in the United States. Androgen deprivation therapy (ADT) is the standard treatment for advanced-stage prostate cancer; however, this treatment eventually fails, leading to an incurable disease subtype known as metastatic castration-resistant prostate cancer (mCRPC). There are several molecular mechanisms that facilitate the development of mCRPC engaging androgen receptor (AR) growth axis, including AR amplification, gain of function AR mutations, and AR splice variants that are constitutively active and are a foremost factor for mCRPC development. AR-independent mechanisms with exceptionally low or absent AR expression found in cancer cells suppress ADT effectiveness and contribute to aggressive variants, including neuroendocrine differentiation. Several other AR regulatory factors such as epigenetic modification(s), and DNA damage response have been reported during post-ADT exposure and play a crucial role in mCRPC development. Therefore, targeting prostate cancer cells before their progression to mCRPC would improve patient outcomes. This special issue in “Cancer Drug Resistance” focuses on understanding the mechanism(s) and development of mCRPC resistance. This special issue also highlights the therapeutic strategies to combat against resistant subtype. This issue comprehensively reviews the mCRPC and delivers the update in the forum of mCRPC resistance development.

show abstract

Section: Article Descriptionmentioning

confidence: 99%

Section: Article Descriptionmentioning

confidence: 99%

New insights for drug resistance in metastatic castration-resistant prostate cancer

Kushwaha¹,

Gupta²

2022

Cancer Drug Resist

View full text Add to dashboard Cite

show abstract

“…ONECUT transcription factor family is involved in tumorigenesis. While ONECUT1 is associated with liver development and differentiation, ONECUT2 regulates cell proliferation, migration, adhesion and differentiation ( Choi et al, 2022 ). Elevated expression levels of ONECUT2 have been reported in various cancers, particularly in NEPC ( Choi et al, 2022 ).…”

Section: Other Transcription Factorsmentioning

confidence: 99%

“…While ONECUT1 is associated with liver development and differentiation, ONECUT2 regulates cell proliferation, migration, adhesion and differentiation ( Choi et al, 2022 ). Elevated expression levels of ONECUT2 have been reported in various cancers, particularly in NEPC ( Choi et al, 2022 ). Therefore, ONECUT2 overexpression marks the onset of cancer progression and metastasis.…”

Section: Other Transcription Factorsmentioning

confidence: 99%

Role of transcription factors and chromatin modifiers in driving lineage reprogramming in treatment-induced neuroendocrine prostate cancer

Sreekumar

Saini

2023

Front. Cell Dev. Biol.

View full text Add to dashboard Cite

Therapy-induced neuroendocrine prostate cancer (NEPC) is a highly lethal variant of prostate cancer that is increasing in incidence with the increased use of next-generation of androgen receptor (AR) pathway inhibitors. It arises via a reversible trans-differentiation process, referred to as neuroendocrine differentiation (NED), wherein prostate cancer cells show decreased expression of AR and increased expression of neuroendocrine (NE) lineage markers including enolase 2 (ENO2), chromogranin A (CHGA) and synaptophysin (SYP). NEPC is associated with poor survival rates as these tumors are aggressive and often metastasize to soft tissues such as liver, lung and central nervous system despite low serum PSA levels relative to disease burden. It has been recognized that therapy-induced NED involves a series of genetic and epigenetic alterations that act in a highly concerted manner in orchestrating lineage switching. In the recent years, we have seen a spurt in research in this area that has implicated a host of transcription factors and epigenetic modifiers that play a role in driving this lineage switching. In this article, we review the role of important transcription factors and chromatin modifiers that are instrumental in lineage reprogramming of prostate adenocarcinomas to NEPC under the selective pressure of various AR-targeted therapies. With an increased understanding of the temporal and spatial interplay of transcription factors and chromatin modifiers and their associated gene expression programs in NEPC, better therapeutic strategies are being tested for targeting NEPC effectively.

show abstract

Reprogramming landscape highlighted by dynamic transcriptomes in therapy-induced neuroendocrine differentiation

Asberry

Liu

Nam

et al. 2022

Computational and Structural Biotechnology Journal

View full text Add to dashboard Cite

ONECUT2 as a key mediator of androgen receptor-independent cell growth and neuroendocrine differentiation in castration-resistant prostate cancer

Cited by 3 publications

References 16 publications

New insights for drug resistance in metastatic castration-resistant prostate cancer

New insights for drug resistance in metastatic castration-resistant prostate cancer

Role of transcription factors and chromatin modifiers in driving lineage reprogramming in treatment-induced neuroendocrine prostate cancer

Reprogramming landscape highlighted by dynamic transcriptomes in therapy-induced neuroendocrine differentiation

Contact Info

Product

Resources

About