Evidence map›Paper›PMID 29569387›Full record

ArticleJournal of cellular and molecular medicine2018

A novel functional polymorphism of GSTM3 reduces clear cell renal cell carcinoma risk through enhancing its expression by interfering miR-556 binding.

Ying Wang, Zi-Ying Yang, Yi-Huan Chen, Feng Li, Han Shen, You Yu, Hao-Yue Huang, Zhen-Ya Shen

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.4field-weighted citation impact, top 40% 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

12 citing papers in PubMed, 15 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.

Ying WangDepartment of Cardiovascular Surgery, First Affiliated Hospital & Institute for Cardiovascular Science, Soochow University, Suzhou, Jiangsu, China.ORCID 0000-0001-6863-8383
Zi-Ying YangDepartment of Cardiovascular Surgery, First Affiliated Hospital & Institute for Cardiovascular Science, Soochow University, Suzhou, Jiangsu, China.
Yi-Huan ChenDepartment of Cardiovascular Surgery, First Affiliated Hospital & Institute for Cardiovascular Science, Soochow University, Suzhou, Jiangsu, China.
Feng LiDepartment of Urinary Surgery, First Affiliated Hospital of Soochow University, Suzhou, Jiangsu, China.
Han ShenDepartment of Cardiovascular Surgery, First Affiliated Hospital & Institute for Cardiovascular Science, Soochow University, Suzhou, Jiangsu, China.
You YuDepartment of Cardiovascular Surgery, First Affiliated Hospital & Institute for Cardiovascular Science, Soochow University, Suzhou, Jiangsu, China.
Hao-Yue HuangDepartment of Cardiovascular Surgery, First Affiliated Hospital & Institute for Cardiovascular Science, Soochow University, Suzhou, Jiangsu, China.
Zhen-Ya ShenDepartment of Cardiovascular Surgery, First Affiliated Hospital & Institute for Cardiovascular Science, Soochow University, Suzhou, Jiangsu, China.
Soochow University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dysregulation of glutathione-S-transferase M3 (GSTM3) has been related to clear cell renal cell carcinoma (ccRCC) in our former study. GSTM3 plays a pivotal role of detoxification and clearance of reactive oxygen species (ROS) in tumour tissues. This study aimed to examine: (1) the associations between GSTM3 single nucleotide polymorphisms (SNPs) and risk of ccRCC, and (2) the potential molecular mechanism accounting for its effects. 5 SNPs in 3'UTR of GSTM3 were initially genotyped in 329 cases and 420 healthy controls. A SNP-rs1055259 was found to be significantly associated with the susceptibility of ccRCC (OR = 0.59, 95% CI = 0.41-0.92; P = .019). The minor allele of rs1055259 (G allele) was associated with RCC risk. This SNP was predicted to affect microRNA (miR)-556 binding to 3'UTR of GSTM3 mRNA. To determine the functional impact, plasmid constructs carrying different alleles of rs1055259 were created. Compared to rs1055259 A-allele constructs, cells transfected with rs1055259 G-allele construct had higher transcriptional activity and were less responsive to miR-556 changes and gene expression. Elevated GSTM3 expression in G-allele cells was associated with ROS activity and ccRCC development. Taken together, this study indicated that a functional polymorphism of GSTM3 -rs1055259 reduced susceptibility of RCC in the Chinese population. It influenced GSTM3 protein synthesis by interfering miR-556 binding, subsequently suppressed ROS activity and ccRCC progression.

Indexed as

Genetic Predisposition to DiseaseAdultAgedAged, 80 and overAllelesCarcinoma, Renal CellCell MovementCell ProliferationFemaleGene Expression Regulation, NeoplasticGenotypeGlutathione TransferaseHumansMaleMicroRNAsMiddle AgedGlutathione TransferaseGSTM3 protein, humanMicroRNAsMIRN556 microRNA, humanRNA-Binding Proteinsclear cell renal cell carcinomaglutathione-S-transferase Mu3invasionmiRNApolymorphism

Identifiers

PMID29569387
PMCPMC5980204
OpenAlexW2794367470

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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.