Evidence map›Paper›PMID 33414441›Full record

ArticleCell death & disease2021

Loss of EHF facilitates the development of treatment-induced neuroendocrine prostate cancer.

Zhi Long, Liang Deng, Chao Li, Qiangrong He, Yao He, Xiheng Hu, Yi Cai, Yu Gan

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.2field-weighted citation impact, top 12% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

12 citing papers in PubMed, 19 citations in OpenAlex.

  1. Review
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  5. Article
  6. Review
  7. Article
  8. Article
  9. Focus on the tumor microenvironment: A seedbed for neuroendocrine prostateFrontiers in cell and developmental biology · 2022
    Review
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  11. Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 1 institution in 1 country.

Zhi LongDepartment of Urology, Andrology Center, The Third Xiangya Hospital, Central South University, Changsha, Hunan, 410013, People's Republic of China.
Liang DengDepartment of Urology, Andrology Center, The Third Xiangya Hospital, Central South University, Changsha, Hunan, 410013, People's Republic of China.
Chao LiDepartment of Urology, Andrology Center, The Third Xiangya Hospital, Central South University, Changsha, Hunan, 410013, People's Republic of China.
Qiangrong HeDepartment of Urology, Andrology Center, The Third Xiangya Hospital, Central South University, Changsha, Hunan, 410013, People's Republic of China.
Yao HeDepartment of Urology, Xiangya Hospital, Central South University, Changsha, Hunan, 410008, People's Republic of China.
Xiheng HuDepartment of Urology, Xiangya Hospital, Central South University, Changsha, Hunan, 410008, People's Republic of China.
Yi CaiDepartment of Urology, Xiangya Hospital, Central South University, Changsha, Hunan, 410008, People's Republic of China.
Yu GanDepartment of Urology, Xiangya Hospital, Central South University, Changsha, Hunan, 410008, People's Republic of China. 148302039@csu.edu.cn.ORCID 0000-0001-9540-6158
Central South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The rising of a highly aggressive subtype of castration-resistant prostate cancer (CRPC) named treatment-induced neuroendocrine prostate cancer (t-NEPC) after androgen deprivation therapy (ADT) is well known for its features of the neuroendocrine differentiation (NED) and androgen receptor (AR) independence. However, t-NEPC is still largely unknown. Here, we found that EHF is notably depressed in t-NEPC tumors, patient-derived xenografts, transgenic mice, and cell models. Results from cell lines uncovered that ADT represses EHF expression, which is required for the ADT-induced NED. Mechanism dissection revealed that ADT decreases the EHF transcription via relieving the AR binding to different androgen-responsive elements, which then promotes the expression and enzymatic activity of enhancer of zeste homolog 2 (EZH2), consequently catalyzing tri-methylation lysine 27 of histone H3 for transcriptional repression of its downstream genes to promote the NED. Furthermore, preclinical studies from cell and mice models proved that recovery of EHF expression or using EZH2 inhibitor can attenuate aggressive properties of CRPC cells, hinder the progression of t-NEPC, and promote the response of CPRC cells to enzalutamide. Together, we elucidate that the ADT/AR/EHF/EZH2 signaling is required for the ADT-enhanced NED and plays a critical role in the progression of t-NEPC.

Indexed as

AnimalsHumansMaleMiceProstatic Neoplasms, Castration-ResistantTranscription FactorsEHF protein, humanTranscription Factors

Identifiers

PMID33414441
PMCPMC7790822
OpenAlexW3118689130

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.