Evidence map›Paper›PMID 35363937›Full record

ArticleMolecular oncology2022

miR-126 downregulates CXCL12 expression in intestinal epithelial cells to suppress the recruitment and function of macrophages and tumorigenesis in a murine model of colitis-associated colorectal cancer.

Shuai Wu, Wei Yuan, Weiwei Luo, Kai Nie, Xing Wu, Xiangrui Meng, Zhaohua Shen, Xiaoyan Wang

Open access · goldAbstract read
In one paragraph

Article in Molecular oncology, 2022. 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
2.4field-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

15 citing papers in PubMed, 26 citations in OpenAlex.

  1. Review
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  4. miR-126: a bridge between cancer and exercise.Cancer cell international · 2025
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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.

Shuai WuDepartment of Gastroenterology, The Third Xiangya Hospital, The Central South University, Changsha, China.ORCID 0000-0003-1818-0831
Wei YuanDepartment of Gastroenterology, The Third Xiangya Hospital, The Central South University, Changsha, China.
Weiwei LuoDepartment of Gastroenterology, The Third Xiangya Hospital, The Central South University, Changsha, China.
Kai NieDepartment of Gastroenterology, The Third Xiangya Hospital, The Central South University, Changsha, China.
Xing WuDepartment of Gastroenterology, The Third Xiangya Hospital, The Central South University, Changsha, China.
Xiangrui MengDepartment of Gastroenterology, The Third Xiangya Hospital, The Central South University, Changsha, China.
Zhaohua ShenDepartment of Gastroenterology, The Third Xiangya Hospital, The Central South University, Changsha, China.
Xiaoyan WangDepartment of Gastroenterology, The Third Xiangya Hospital, The Central South University, Changsha, China.
Central South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Inflammatory bowel disease, characterised by chronic relapsing-remitting colitis, is a significant risk factor for colorectal cancer (CRC). Previously, we showed that miR-126 functions as a tumour suppressor in CRC and is inversely correlated with tumour proliferation, metastasis and patient prognosis. In the current study, we documented a protective role for miR-126 in colitis-associated CRC (CAC) and its underlying mechanism. We detected downregulated miR-126 expression during colorectal tumorigenesis in the mouse CAC model and in specimens from patients with CRC. The deficiency of miR-126 in intestinal epithelial cells (IECs) exacerbated tumorigenesis in mice. We identified CXCL12 as a direct target of miR-126 in inhibiting the development of colitis and CAC. Moreover, miR-126 regulated the recruitment of macrophages via CXCL12 and decreased the levels of proinflammatory cytokines (IL-6, IL-12 and IL-23). In addition, IL-6 secreted by macrophages, which were regulated by cocultured transfected CRC cells, altered the proliferation and migration of colon cells. Our data suggest that miR-126 exerts an antitumour effect on CAC by regulating the crosstalk between IECs and macrophages via CXCL12-IL-6 signalling. Our study contributes to the understanding of cancer progression and suggests miR-126 as a potential therapy for CRC.

Indexed as

ColitisColitis-Associated NeoplasmsColorectal NeoplasmsMicroRNAsAnimalsCarcinogenesisCell ProliferationCell Transformation, NeoplasticCytokinesDisease Models, AnimalEpithelial CellsInterleukin-12Interleukin-23Interleukin-6MacrophagesMiceCytokinesInterleukin-12Interleukin-23Interleukin-6MicroRNAscolorectal cancerCXCL12intestinal epithelial cellsmacrophagesmiR-126

Identifiers

PMID35363937
PMCPMC9533691
OpenAlexW4220789245

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.