Evidence map›Paper›PMID 36038573›Full record

ArticleCell death & disease2022

High dose androgen suppresses natural killer cytotoxicity of castration-resistant prostate cancer cells via altering AR/circFKBP5/miRNA-513a-5p/PD-L1 signals.

Min Tang, Yin Sun, Chi-Ping Huang, Lei Chen, Bianjiang Liu, Bosen You, Zengjun Wang, Chawnshang Chang

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

20 citing papers in PubMed, 22 citations in OpenAlex.

  1. Review
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  4. Hsa_circ_0030568 Promotes the Proliferation and Migration of Prostate Cancer CellsCombinatorial chemistry & high throughput screening · 2026
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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 4 institutions in 3 countries.

Min Tang *Department of Urology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu, 210000, China.
Yin Sun *George Whipple Lab for Cancer Research, Departments of Pathology, Urology, Radiation Oncology and The Wilmot Cancer Institute, University of Rochester Medical Center, Rochester, 14642 NY, USA.
Chi-Ping Huang *Department of Urology, China Medical University/Hospital, Taichung, 404, Taiwan.ORCID 0000-0003-1429-1366
Lei Chen *George Whipple Lab for Cancer Research, Departments of Pathology, Urology, Radiation Oncology and The Wilmot Cancer Institute, University of Rochester Medical Center, Rochester, 14642 NY, USA.
Bianjiang LiuDepartment of Urology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu, 210000, China.ORCID 0000-0002-4705-6445
Bosen YouGeorge Whipple Lab for Cancer Research, Departments of Pathology, Urology, Radiation Oncology and The Wilmot Cancer Institute, University of Rochester Medical Center, Rochester, 14642 NY, USA.ORCID 0000-0002-9037-2136
Zengjun WangDepartment of Urology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu, 210000, China. zengjunwang@njmu.edu.cn.
Chawnshang ChangGeorge Whipple Lab for Cancer Research, Departments of Pathology, Urology, Radiation Oncology and The Wilmot Cancer Institute, University of Rochester Medical Center, Rochester, 14642 NY, USA. Chang@urmc.rochester.edu.ORCID 0000-0001-8510-3516
University of Rochester Medical Center · USChina Medical University · TWAnhui Medical University · CNJiangsu Province Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Most advanced prostate cancer (PCa) patients initially respond well to androgen deprivation therapy, but almost all eventually develop castration-resistant prostate cancer (CRPC). Early studies indicated the bipolar androgen therapy via a cycling of high dose and low dose of androgen to suppress PCa growth might be effective in a select patient population. The detailed mechanisms, however, remain unclear. Here we found the capacity of natural killer (NK) cells to suppress the CRPC cells could be suppressed by a high dose of dihydrotestosterone (DHT). Mechanism dissection indicates that transactivated AR can increase circularRNA-FKBP5 (circFKBP5) expression, which could sponge/inhibit miR-513a-5p that suppresses the PD-L1 expression via direct binding to its 3'UTR to negatively impact immune surveillance from NK cells. Preclinical data from in vitro cell lines and an in vivo mouse model indicate that targeting PD-L1 with sh-RNA or anti-PD-L1 antibody can enhance the high dose DHT effect to better suppress CRPC cell growth. These findings may help us to develop novel therapies via combination of high dose androgen with PD-1/PD-L1 checkpoint inhibitors to better suppress CRPC progression.

Indexed as

MicroRNAsProstatic Neoplasms, Castration-ResistantAndrogen AntagonistsAndrogensAnimalsCell Line, TumorDihydrotestosteroneHumansKiller Cells, NaturalMaleMiceReceptors, AndrogenAndrogen AntagonistsAndrogensDihydrotestosteroneMicroRNAsReceptors, Androgen

Identifiers

PMID36038573
PMCPMC9424293
OpenAlexW4293434526

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.