Evidence map›Paper›PMID 30561001›Full record

ArticleInternational journal of cancer2019

Genetic variants in SLC22A3 contribute to the susceptibility to colorectal cancer.

Anjing Ren, Shanwen Sun, Shuwei Li, Tao Chen, Yongqian Shu, Mulong Du, Lingjun Zhu

Open access · hybridAbstract read
In one paragraph

Article in International journal of cancer, 2019. 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
2.4field-weighted citation impact, top 10% 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, 26 citations in OpenAlex.

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  15. Genetic and Epigenetic Regulation of Organic Cation Transporters.Handbook of experimental pharmacology · 2021
    Review
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  17. Review
  18. Review
  19. Article
  20. Article
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

7 authors at 3 institutions in 2 countries.

Anjing RenDepartment of Oncology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Shanwen SunDepartment of Oncology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Shuwei LiDepartment of Environmental Genomics, Jiangsu Key Laboratory of Cancer Biomarkers, Prevention and Treatment, Collaborative Innovation Center For Cancer Personalized Medicine, Nanjing Medical University, Nanjing, China.
Tao ChenDepartment of General Surgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Yongqian ShuDepartment of Oncology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Mulong DuDepartment of Environmental Genomics, Jiangsu Key Laboratory of Cancer Biomarkers, Prevention and Treatment, Collaborative Innovation Center For Cancer Personalized Medicine, Nanjing Medical University, Nanjing, China.
Lingjun ZhuDepartment of Oncology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.ORCID 0000-0001-8033-1528
Jiangsu Province Hospital · CNJiangsu Cancer Hospital · CNMinistry of Education · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Previous a genome-wide association study (GWAS) of colorectal cancer in Japanese population has identified a risk region at the chromosome 6q26-q27 associated with colorectal cancer risk. However, the causal gene at this locus remained unclear. In our study, we enrolled a total of 14 candidate functional single nucleotide polymorphisms (SNPs) at 6q26-q27 (318 kb), and then genotyped them by TaqMan method in a Chinese population including 1,147 colorectal cancer cases and 1,203 controls. Among that, 5 SNPs were identified statistical association with colorectal cancer risk by logistic regression analysis. Of which, SNP rs420038 G > A in SLC22A3 was related to decreased risk of colorectal cancer (adjusted odds ratio (OR) = 0.79, 95% confidence interval (CI) = 0.67-0.94, p = 0.007), and also associated with lower expression of SLC22A3 (p = 0.040) using expression quantitative trait loci (eQTL) analysis. Moreover, by the luciferase assays, we found that compared to the G allele of rs420038, the A allele could suppress the activity of the promoter in SLC22A3. Furthermore, the expression of SLC22A3 was significantly higher in colorectal cancer tissues than that in paired normal tissues (p < 0.001). Meanwhile, the phenotypes of proliferation, migration, invasion, cell cycle and apoptosis of colorectal cancer cell were significantly affected by SLC22A3 in vitro. Our results revealed a novel susceptible locus, rs420038 in SLC22A3, which may be involved in colorectal cancer development and progression.

Indexed as

Asian PeopleCell DeathCell ProliferationChromosomes, Human, Pair 6Colorectal NeoplasmsEthnicityFemaleGenetic Predisposition to DiseaseGenome-Wide Association StudyGenotypeHumansMaleMiddle AgedOrganic Cation Transporter 3Organic Cation Transport ProteinsPolymorphism, Single NucleotideOrganic Cation Transporter 3Organic Cation Transport Proteinscolorectal cancergenetic variantsSLC22A3susceptibility

Identifiers

PMID30561001
PMCPMC6590332
OpenAlexW2904391634

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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.