Evidence map›Paper›PMID 33109107›Full record

ArticleBMC cancer2020

miR-203 inhibits cell proliferation and ERK pathway in prostate cancer by targeting IRS-1.

Yang Meng, Xiaoyan Hu, Shasha Li, Xinyi Zeng, Lei Qiu, Mingtian Wei, Ziqing Wang, Junhong Han

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.4field-weighted citation impact, top 21% 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

16 citing papers in PubMed, 27 citations in OpenAlex.

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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 1 institution in 1 country.

Yang MengDepartment of Abdominal Oncology and Laboratory of Epigenetics, State Key Laboratory of Biotherapy and Cancer Center, West China Hospital, Sichuan University, Chengdu, 610041, P.R. China.
Xiaoyan HuDepartment of Abdominal Oncology and Laboratory of Epigenetics, State Key Laboratory of Biotherapy and Cancer Center, West China Hospital, Sichuan University, Chengdu, 610041, P.R. China.
Shasha LiDepartment of Abdominal Oncology and Laboratory of Epigenetics, State Key Laboratory of Biotherapy and Cancer Center, West China Hospital, Sichuan University, Chengdu, 610041, P.R. China.
Xinyi ZengDepartment of Abdominal Oncology and Laboratory of Epigenetics, State Key Laboratory of Biotherapy and Cancer Center, West China Hospital, Sichuan University, Chengdu, 610041, P.R. China.
Lei QiuDepartment of Abdominal Oncology and Laboratory of Epigenetics, State Key Laboratory of Biotherapy and Cancer Center, West China Hospital, Sichuan University, Chengdu, 610041, P.R. China.
Mingtian WeiDepartment of Gastrointestinal Surgery, West China Hospital, Sichuan University, Chengdu, 610041, P.R. China.
Ziqing WangDepartment of Gastrointestinal Surgery, West China Hospital, Sichuan University, Chengdu, 610041, P.R. China.
Junhong HanDepartment of Abdominal Oncology and Laboratory of Epigenetics, State Key Laboratory of Biotherapy and Cancer Center, West China Hospital, Sichuan University, Chengdu, 610041, P.R. China. hjunhong@scu.edu.cn.ORCID http://orcid.org/0000-0002-3371-8698
Sichuan University · CN

Funding

Department of Science and Technology of Sichuan Province 2018JY0018Innovative Research Group Project of the National Natural Science Foundation of China 81820012National Natural Science Foundation of China 81672782,31972884
6 · The paper itself

Abstract

introductionProstate cancer (PCa) is one of the most common types of cancer in men. In the course of the development and progression of this disease, abnormal expression of miR-203 is usually accompanied. However, its role in prostate tumorigenesis and the underlying mechanism are poorly understood.

methodsDual luciferase reporter gene analysis was used to detect miR-203 binding site in insulin receptor substrates 1 (IRS-1). Cell proliferation was assessed by MTT assay in PCa cells with either IRS-1 knockdown or miR-203 overexpression. IRS-1 and other proteins expression in PCa cells was assessed by Western Blot.

resultswe found that the insulin receptor substrates 1 (IRS-1) is a novel target of miR-203 in PCa and miR-203 can specifically bind to the 3'UTR region of the IRS-1 thus suppresses its expression. Moreover, we demonstrate that miR-203 functions as a tumor suppressor by directly targeting IRS-1 to inhibit cell proliferation and migration which results in PCa cell cycle arrest. Importantly, miR-203 overexpression blocks ERK signalling pathway by down-regulating IRS-1 expression.

conclusionsOur results show a novel link between miR-203 and IRS-1, and reveal the importance of strict control of IRS - 1 by miR-203 in the progression of PCa, suggesting miR-203 may act as a promising target for the diagnosis and treatment of advanced PCa.

Indexed as

3' Untranslated RegionsCell Line, TumorCell ProliferationGene Expression Regulation, NeoplasticHumansInsulin Receptor Substrate ProteinsMaleMAP Kinase Signaling SystemMicroRNAsNeoplasm MetastasisProstatic Neoplasms3' Untranslated RegionsInsulin Receptor Substrate ProteinsIRS1 protein, humanMicroRNAsMIRN203 microRNA, humanCell proliferationERK pathwayInsulin receptor substrates 1 (IRS-1)miRNAProstate cancer

Identifiers

PMID33109107
PMCPMC7590475
OpenAlexW2966731060

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.