Evidence map›Paper›PMID 34323404›Full record

ArticleClinical and translational medicine2021

Histone acetyltransferase 1 upregulates androgen receptor expression to modulate CRPC cell resistance to enzalutamide.

Zhe Hong, Zhendong Xiang, Pan Zhang, Qiang Wu, Chengdang Xu, Xinan Wang, Guowei Shi, Zongyuan Hong, Denglong Wu

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Clinical and translational medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
3.7field-weighted citation impact, top 6% 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

19 citing papers in PubMed, 31 citations in OpenAlex.

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  13. Targeting epigenetic regulators to overcome drug resistance in cancers.Signal transduction and targeted therapy · 2023
    Review
  14. The epigenetic function of androgen receptor in prostate cancer progression.Frontiers in cell and developmental biology · 2023
    Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 2 institutions in 2 countries.

Zhe HongDepartment of Urology, Tongji Hospital, School of Medicine, Tongji University, Shanghai, China.
Zhendong XiangDepartment of Urology, Tongji Hospital, School of Medicine, Tongji University, Shanghai, China.
Pan ZhangIllinois Informatics Institute, University of Illinois at Urbana-Champaign, Champaign, Illinois, USA.
Qiang WuDepartment of Urology, Tongji Hospital, School of Medicine, Tongji University, Shanghai, China.
Chengdang XuDepartment of Urology, Tongji Hospital, School of Medicine, Tongji University, Shanghai, China.
Xinan WangDepartment of Urology, Tongji Hospital, School of Medicine, Tongji University, Shanghai, China.
Guowei ShiDepartment of Urology, the Fifth People's Hospital of Shanghai, Urology Research Center of Fudan University, Shanghai, China.
Zongyuan HongLaboratory of Quantitative Pharmacology, Wannan Medical College, Wuhu, China.ORCID 0000-0001-5942-4893
Denglong WuDepartment of Urology, Tongji Hospital, School of Medicine, Tongji University, Shanghai, China.
Tongji University · CNWannan Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Castration-resistant prostate cancer (CRPC) is the latest stage of PCa, and there is almost no effective treatment available for the patients with CRPC when next-generation androgen deprivation therapy drugs, such as enzalutamide (ENZ), fail. The androgen receptor (AR) plays key roles in PCa and CRPC progression and drug resistance. Histone acetyltransferase 1 (HAT1) has recently been reported to be highly expressed in some tumors, such as lung carcinoma. However, what relationship between the AR and HAT1, and whether or how HAT1 plays roles in CRPC progression and drug resistance remain elusive. In the present study, we found that HAT1 is highly expressed in PCa cells, and the overexpression of HAT1 is linked with CRPC cell proliferation. Moreover, the HAT1 expression is positively correlated with the expression of AR, including both AR-FL (full-length) and AR-V7 (variant 7), which is mainly mediated by a bromodomain containing protein 4 (BRD4) -mediated pathway. Furthermore, knockdown of HAT1 can re-sensitize the response of CRPC cells to ENZ treatment in cells and mouse models. In addition, ascorbate was observed to decrease AR expression through downregulation of HAT1 expression. Collectively, our findings reveal a novel AR signaling regulation pathway in PCa and CRPC and suggest that HAT1 serves as a critical oncoprotein and an ideal target for the treatment of ENZ resistance in CRPC patients.

Indexed as

AnimalsAntineoplastic AgentsBenzamidesBromodomain Containing ProteinsCell Cycle ProteinsCell Line, TumorCell MovementCell ProliferationHistone AcetyltransferasesHumansMaleMiceMice, Inbred NODNitrilesPhenylthiohydantoinProstatic Neoplasms, Castration-ResistantAntineoplastic AgentsBenzamidesBRD4 protein, humanBromodomain Containing ProteinsCell Cycle ProteinsenzalutamideHistone Acetyltransferaseshistone acetyltransferase type B complexNitrilesPhenylthiohydantoinReceptors, AndrogenRNA, Small InterferingTranscription Factorsandrogen receptorbromodomain containing protein 4castration-resistant prostate cancerenzalutamidehistone acetyltransferase 1

Identifiers

PMID34323404
PMCPMC8299045
OpenAlexW3186797593

What OpenQuestion holds

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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.