Evidence map›Paper›PMID 36408179›Full record

ArticleFrontiers in oncology2022

Increased

Maryam Labaf, Muqing Li, Lily Ting, Breelyn Karno, Songqi Zhang, Shuai Gao, Susan Patalano, Jill A Macoska, Kourosh Zarringhalam, Dong Han and 1 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in oncology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.3field-weighted citation impact, top 10% 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

14 citing papers in PubMed, 17 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
  5. Review
  6. Review
  7. Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Review
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

11 authors at 3 institutions in 1 country.

Maryam LabafCenter for Personalized Cancer Therapy, University of Massachusetts Boston, Boston, MA, United States.
Muqing LiCenter for Personalized Cancer Therapy, University of Massachusetts Boston, Boston, MA, United States.
Lily TingCenter for Personalized Cancer Therapy, University of Massachusetts Boston, Boston, MA, United States.
Breelyn KarnoDepartment of Medicine, Vanderbilt University, Nashville, TN, United States.
Songqi ZhangCenter for Personalized Cancer Therapy, University of Massachusetts Boston, Boston, MA, United States.
Shuai GaoDepartment of Cell Biology and Anatomy, New York Medical College, Valhalla, NY, United States.
Susan PatalanoCenter for Personalized Cancer Therapy, University of Massachusetts Boston, Boston, MA, United States.
Jill A MacoskaCenter for Personalized Cancer Therapy, University of Massachusetts Boston, Boston, MA, United States.
Kourosh ZarringhalamDepartment of Mathematics, University of Massachusetts Boston, Boston, MA, United States.
Dong HanCenter for Personalized Cancer Therapy, University of Massachusetts Boston, Boston, MA, United States.
Changmeng CaiCenter for Personalized Cancer Therapy, University of Massachusetts Boston, Boston, MA, United States.
University of Massachusetts Boston · USNew York Medical College · USVanderbilt University · US

Funding

UMass Boston-DF/HCC U54 Partnership (2 of 2)U54CA156734 · NCI · UNIVERSITY OF MASSACHUSETTS BOSTON · PI ADAN COLON-CARMONA, Jill A. Macoska · 2010 to 2026
$24.9M
Study the Mechanism of Retinoblastoma Protein Mediated Androgen Receptor Transcriptional Repression Activity on DNA ReplicationR01CA211350 · NCI · UNIVERSITY OF MASSACHUSETTS BOSTON · PI CAI, CHANGMENG · 2017 to 2021
$1.7M
NCI NIH HHS R01 CA211350NCI NIH HHS U54 CA156734
6 · The paper itself

Abstract

Elevated androgen receptor (AR) expression is a hallmark of castration-resistant prostate cancer (CRPC) and contributes to the restoration of AR signaling under the conditions of androgen deprivation. However, whether overexpressed AR alone with the stimulation of castrate levels of androgens can be sufficient to induce the reprogramming of AR signaling for the adaptation of prostate cancer (PCa) cells remains unclear. In this study, we used a PCa model with inducible overexpression of AR to examine the acute effects of AR overexpression on its cistrome and transcriptome. Our results show that overexpression of AR alone in conjunction with lower androgen levels can rapidly redistribute AR chromatin binding and activates a distinct transcription program that is enriched for DNA damage repair pathways. Moreover, using a recently developed bioinformatic tool, we predicted the involvement of EZH2 in this AR reprogramming and subsequently identified a subset of AR/EZH2 co-targeting genes, which are overexpressed in CRPC and associated with worse patient outcomes. Mechanistically, we found that AR-EZH2 interaction is impaired by the pre-castration level of androgens but can be recovered by the post-castration level of androgens. Overall, our study provides new molecular insights into AR signaling reprogramming with the engagement of specific epigenetic factors.

Indexed as

androgenandrogen-deprivation therapyandrogen receptorARCRPCDNA damage repairEZH2prostate cancer

Identifiers

PMID36408179
PMCPMC9669968
OpenAlexW4308416697

What OpenQuestion holds

Textmetadata
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.