Evidence map›Paper›PMID 25742789›Full record

ArticleOncotarget2015

Up-regulation of matrix metalloproteinases in a mouse model of chemically induced colitis-associated cancer: the role of microRNAs.

Feiyan Ai, Xuemei Zhang, Xiayu Li, Zailong Qin, Qiurong Ye, Li Tian, Anliu Tang, Nan Li, Guiyuan Li, Jian Ma and 1 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.1field-weighted citation impact, top 14% 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

15 citing papers in PubMed, 27 citations in OpenAlex.

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  14. Matrix metalloproteinase-12 expression is increased in cutaneous melanoma and associated with tumor aggressiveness.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015
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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

11 authors at 3 institutions in 1 country.

Feiyan AiDepartment of Gastroenterology, The Third Xiangya Hospital of Central South University, Changsha, Hunan, China.
Xuemei ZhangDepartment of Gastroenterology, The Third Xiangya Hospital of Central South University, Changsha, Hunan, China.
Xiayu LiDepartment of Gastroenterology, The Third Xiangya Hospital of Central South University, Changsha, Hunan, China.
Zailong QinHunan Cancer Hospital and the Affiliated Cancer Hospital of Xiangya School of Medicine, Cancer Research Institute, Central South University, Key Laboratory of Carcinogenesis, Ministry of Health, Key Laboratory of Carcinogenesis and Cancer Invasion, Ministry of Education, Changsha, Hunan, China.
Qiurong YeHunan Cancer Hospital and the Affiliated Cancer Hospital of Xiangya School of Medicine, Cancer Research Institute, Central South University, Key Laboratory of Carcinogenesis, Ministry of Health, Key Laboratory of Carcinogenesis and Cancer Invasion, Ministry of Education, Changsha, Hunan, China.
Li TianDepartment of Gastroenterology, The Third Xiangya Hospital of Central South University, Changsha, Hunan, China.
Anliu TangDepartment of Gastroenterology, The Third Xiangya Hospital of Central South University, Changsha, Hunan, China.
Nan LiDepartment of Gastroenterology, The Third Xiangya Hospital of Central South University, Changsha, Hunan, China.
Guiyuan LiHunan Key Laboratory of Nonresolving Inflammation and Cancer, Changsha, Hunan, China.
Jian MaHunan Key Laboratory of Nonresolving Inflammation and Cancer, Changsha, Hunan, China.
Shourong ShenDepartment of Gastroenterology, The Third Xiangya Hospital of Central South University, Changsha, Hunan, China.
Central South University · CNThird Xiangya Hospital · CNHunan Cancer Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Emerging evidence has implicated microRNAs in regulating the production of multiple inflammatory mediators including cytokines and chemokines. We previously elucidated the dynamic activation of key signals that link colitis to colorectal cancer. In this study, we observed a sharp increase in the levels of matrix metalloproteinases (Mmps) that provided a basis for the inflammation-cancer link, and we questioned whether this was a consequence of the dysregulation of Mmp-specific microRNAs, at least partly. We assayed a panel of murine microRNAs that were predicted to target Mmps and found they were downregulated in the inflammation-cancer link. Furthermore, we demonstrated that three murine microRNAs, namely miR-128, -134, and -330, can target the three Mmps Mmp3, Mmp10, and Mmp13, respectively. We also found that the level of the microRNA-processing enzyme Dicer1 was decreased in the inflammation-cancer link. These microRNAs functioned as tumor suppressors in colon cancer cells, attenuating the proliferation, migration, and invasion potential of murine colon cancer cells as well as angiogenesis and the growth of tumors derived from these cells. Our results suggest that microRNAs modulate the production of key inflammatory mediators and that microRNA dysfunction may contribute to the non-resolving inflammation associated with cancer.

Indexed as

Neovascularization, PathologicAnimalsApoptosisBlotting, WesternCell MovementCell ProliferationCells, CulturedColitisColonic NeoplasmsHumansHuman Umbilical Vein Endothelial CellsImmunoenzyme TechniquesLipopolysaccharidesMaleMatrix MetalloproteinasesMiceLipopolysaccharidesMatrix MetalloproteinasesMicroRNAsRNA, Messengercolitis-associated cancerDicer1matrix metalloproteinasesmicroRNAsnon-resolving inflammation

Identifiers

PMID25742789
PMCPMC4467157
OpenAlexW1740988218

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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.