Evidence map›Paper›PMID 33390173›Full record

ArticleJournal of experimental & clinical cancer research : CR2021

ASC-J9® suppresses prostate cancer cell proliferation and invasion via altering the ATF3-PTK2 signaling.

Hao Tian, Fu-Ju Chou, Jing Tian, Yong Zhang, Bosen You, Chi-Ping Huang, Shuyuan Yeh, Yuanjie Niu, Chawnshang Chang

Open access · goldAbstract read
In one paragraph

Article in Journal of experimental & clinical cancer research : CR, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

10 citing papers in PubMed, 19 citations in OpenAlex.

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  8. Recent advances on the mechanisms of kidney stone formation (Review).International journal of molecular medicine · 2021
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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

9 authors at 4 institutions in 3 countries.

Hao TianDepartment of Urology, Tianjin Institute of Urology, The Second Hospital of Tianjin Medical University, Tianjin Medical University, Tianjin, 300211, China.
Fu-Ju ChouGeorge Whipple Lab for Cancer Research, Departments of Pathology and Urology, University of Rochester Medical Center, Rochester, NY, 14642, USA.
Jing TianDepartment of Urology, Tianjin Institute of Urology, The Second Hospital of Tianjin Medical University, Tianjin Medical University, Tianjin, 300211, China.
Yong ZhangDepartment of Urology, the Second Hospital of Hebei Medical University, Shijiazhuang, 050000, China.
Bosen YouGeorge Whipple Lab for Cancer Research, Departments of Pathology and Urology, University of Rochester Medical Center, Rochester, NY, 14642, USA.
Chi-Ping HuangSex Hormone Research Center, Department of Urology, China Medical University, Taichung, 404, Taiwan.
Shuyuan YehGeorge Whipple Lab for Cancer Research, Departments of Pathology and Urology, University of Rochester Medical Center, Rochester, NY, 14642, USA.
Yuanjie NiuDepartment of Urology, Tianjin Institute of Urology, The Second Hospital of Tianjin Medical University, Tianjin Medical University, Tianjin, 300211, China. niuyuanjie9317@163.com.
Chawnshang ChangGeorge Whipple Lab for Cancer Research, Departments of Pathology and Urology, University of Rochester Medical Center, Rochester, NY, 14642, USA. chang@urmc.rochester.edu.
University of Rochester Medical Center · USChina Medical University · TWSecond Hospital of Tianjin Medical University · CNSecond Hospital of Hebei Medical University · CN

Funding

China Sponsorship Council 201606940026
6 · The paper itself

Abstract

backgroundEarly studies indicated that ASC-J9®, an androgen receptor (AR) degradation enhancer, could suppress the prostate cancer (PCa) progression. Here we found ASC-J9® could also suppress the PCa progression via an AR-independent mechanism, which might involve modulating the tumor suppressor ATF3 expression.

methodsThe lentiviral system was used to modify gene expression in C4-2, CWR22Rv1 and PC-3 cells. Western blot and Immunohistochemistry were used to detect protein expression. MTT and Transwell assays were used to test the proliferation and invasion ability.

resultsASC-J9® can suppress PCa cell proliferation and invasion in both PCa C4-2 and CWR22Rv1 cells via altering the ATF3 expression. Further mechanistic studies reveal that ASC-J9® can increase the ATF3 expression via decreasing Glutamate-cysteine ligase catalytic (GCLC) subunit expression, which can then lead to decrease the PTK2 expression. Human clinical studies further linked the ATF3 expression to the PCa progression. Preclinical studies using in vivo mouse model also proved ASC-J9® could suppress AR-independent PCa cell invasion, which could be reversed after suppressing ATF3.

conclusionsASC-J9® can function via altering ATF3/PTK2 signaling to suppress the PCa progression in an AR-independent manner.

Indexed as

Activating Transcription Factor 3AnimalsCell Line, TumorCell ProliferationCurcuminFocal Adhesion Kinase 1HumansMaleMiceMice, NudeNeoplasm InvasivenessProstatic NeoplasmsSignal TransductionXenograft Model Antitumor AssaysActivating Transcription Factor 3ASC-J9 compoundATF3 protein, humanCurcuminFocal Adhesion Kinase 1PTK2 protein, humanASC-J9®ATF3ATF3 response elementProstate cancerPTK2

Identifiers

PMID33390173
PMCPMC7780640
OpenAlexW3120244393

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.