Evidence map›Paper›PMID 31000693›Full record

ArticleCell death & disease2019

Androgen receptor regulates ASS1P3/miR-34a-5p/ASS1 signaling to promote renal cell carcinoma cell growth.

Kefeng Wang, Yin Sun, Changcheng Guo, Tao Liu, Xiang Fei, Chawnshang Chang

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.5field-weighted citation impact, top 20% 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

26 citing papers in PubMed, 40 citations in OpenAlex.

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  7. The influence of sex hormones on renal cell carcinoma.Therapeutic advances in medical oncology · 2024
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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

6 authors at 2 institutions in 2 countries.

Kefeng WangDepartment of Urology, Shengjing Hospital, China Medical University, 110004, Shenyang, China.
Yin SunGeorge Whipple Lab for Cancer Research, Departments of Pathology, Urology, Radiation Oncology and The Wilmot Cancer Institute, University of Rochester Medical Center, Rochester, NY, 14642, USA.
Changcheng GuoGeorge Whipple Lab for Cancer Research, Departments of Pathology, Urology, Radiation Oncology and The Wilmot Cancer Institute, University of Rochester Medical Center, Rochester, NY, 14642, USA.
Tao LiuDepartment of Urology, Shengjing Hospital, China Medical University, 110004, Shenyang, China.
Xiang FeiDepartment of Urology, Shengjing Hospital, China Medical University, 110004, Shenyang, China. feixiangurology@126.com.
Chawnshang ChangGeorge Whipple Lab for Cancer Research, Departments of Pathology, Urology, Radiation Oncology and The Wilmot Cancer Institute, University of Rochester Medical Center, Rochester, NY, 14642, USA. chang@urmc.rochester.edu.
China Medical University · CNUniversity of Rochester Medical Center · US

Funding

Non-AR mediated DHT-promoted Bladder Cancer initiation and progressionR01CA155477 · NCI · UNIVERSITY OF ROCHESTER · PI CHANG, CHAWNSHANG · 2011 to 2015
$1.6M
Stromal AR Roles in Prostate Hyperplasia and CancerR01CA156700 · NCI · UNIVERSITY OF ROCHESTER · PI CHANG, CHAWNSHANG, YEH, SHUYUAN · 2011 to 2015
$1.6M
NCI NIH HHS R01 CA155477NCI NIH HHS R01 CA156700
6 · The paper itself

Abstract

Recent studies have demonstrated that the androgen receptor (AR) could play important roles to promote renal cell carcinoma (RCC) cell proliferation, and other studies have also indicated that suppressing the argininosuccinate synthase 1 (ASS1) could promote proliferation of various tumors. The potential of AR promoting cell proliferation in RCC via altering ASS1, however, remains unclear. Here we found that the expression of ASS1 was lower in RCC tissues than in adjacent normal renal tissues, and a lower ASS1 expression was linked to a worse prognosis in RCC patients. Mechanism dissection showed that AR could decrease ASS1 expression to promote RCC cell proliferation via ASS1P3, a pseudogene of ASS1. The results of RIP assay and AGO2 assay revealed that AR could bind ASS1P3 to increase RCC cell proliferation via altering miR-34a-5p function, which could bind to the 3'UTR of ASS1 to suppress its protein expression. ASS1P3 could function as a miRNA decoy for miR-34a-5p to regulate ASS1 in RCC. Preclinical study also supports the in vitro data. Together, these results demonstrated that ASS1P3 could function as a competing endogenous RNA to suppress RCC cell progression, and targeting this newly identified AR-mediated ASS1P3/miR-34a-5p/ASS1 signaling might help in blocking proliferation.

Indexed as

Cell ProliferationSignal Transduction3' Untranslated RegionsAnimalsArgininosuccinate SynthaseCarcinoma, Renal CellCell Line, TumorDisease-Free SurvivalHumansKidney NeoplasmsMiceMice, NudeMicroRNAsReceptors, AndrogenRNA InterferenceRNA, Small Interfering3' Untranslated RegionsArgininosuccinate SynthaseMicroRNAsMIRN34 microRNA, humanReceptors, AndrogenRNA, Small Interfering

Identifiers

PMID31000693
PMCPMC6472417
OpenAlexW2937094540

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.