Evidence map›Paper›PMID 35443745›Full record

ArticleCell death & disease2022

Exosomal miR-146a-5p and miR-155-5p promote CXCL12/CXCR7-induced metastasis of colorectal cancer by crosstalk with cancer-associated fibroblasts.

Dong Wang, Xiaohui Wang, Yujia Song, Mahan Si, Yuqi Sun, Xiaohui Liu, Shuxiang Cui, Xianjun Qu, Xinfeng Yu

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell death & disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 105 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
105citing papers in PubMed, 1 pooled it
15.1field-weighted citation impact, top 1% 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

105 citing papers in PubMed, 1 synthesis or guideline pooled it, 151 citations in OpenAlex.

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45 more citing papers are in PubMed but not listed here.

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

9 authors at 1 institution in 1 country.

Dong Wang *Department of Pharmacology, School of Basic Medical Sciences, Capital Medical University, Beijing, China.
Xiaohui Wang *Department of General Surgery, Xuanwu Hospital, Capital Medical University, Beijing, China.
Yujia Song *Department of Pharmacology, School of Basic Medical Sciences, Capital Medical University, Beijing, China.
Mahan SiDepartment of Pharmacology, School of Basic Medical Sciences, Capital Medical University, Beijing, China.
Yuqi SunDepartment of Pharmacology, School of Basic Medical Sciences, Capital Medical University, Beijing, China.
Xiaohui LiuDepartment of Pharmacology, School of Basic Medical Sciences, Capital Medical University, Beijing, China.
Shuxiang CuiDepartment of Toxicology and Sanitary Chemistry, School of Public Health, Capital Medical University, Beijing, China.ORCID 0000-0002-4466-6045
Xianjun QuDepartment of Pharmacology, School of Basic Medical Sciences, Capital Medical University, Beijing, China.
Xinfeng YuDepartment of Pharmacology, School of Basic Medical Sciences, Capital Medical University, Beijing, China. xyu@ccmu.edu.cn.ORCID 0000-0002-2703-4361
Capital Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

C-X-C motif chemokine receptor 7 (CXCR7) is a newly discovered atypical chemokine receptor that binds to C-X-C motif chemokine ligand 12 (CXCL12) with higher affinity than CXCR4 and is associated with the metastasis of colorectal cancer (CRC). Cancer-associated fibroblasts (CAFs) have been known to promote tumor progression. However, whether CAFs are involved in CXCR7-mediated metastasis of CRC remains elusive. We found a significant positive correlation between CXCR7 expression and CAF activation markers in colonic tissues from clinical specimens and in villin-CXCR7 transgenic mice. RNA sequencing revealed a coordinated increase in the levels of miR-146a-5p and miR-155-5p in CXCR7-overexpressing CRC cells and their exosomes. Importantly, these CRC cell-derived miR-146a-5p and miR-155-5p could be uptaken by CAFs via exosomes and promote the activation of CAFs through JAK2-STAT3/NF-κB signaling by targeting suppressor of cytokine signaling 1 (SOCS1) and zinc finger and BTB domain containing 2 (ZBTB2). Reciprocally, activated CAFs further potently enhanced the invasive capacity of CRC cells. Mechanistically, CAFs transfected with miR-146a-5p and miR-155-5p exhibited a robust increase in the levels of inflammatory cytokines interleukin-6, tumor necrosis factor-α, transforming growth factor-β, and CXCL12, which trigger the epithelial-mesenchymal transition and pro-metastatic switch of CRC cells. More importantly, the activation of CAFs by miR-146a-5p and miR-155-5p facilitated tumor formation and lung metastasis of CRC in vivo using tumor xenograft models. Our work provides novel insights into CXCR7-mediated CRC metastasis from tumor-stroma interaction and serum exosomal miR-146a-5p and miR-155-5p could serve as potential biomarkers and therapeutic targets for inhibiting CRC metastasis.

Indexed as

Cancer-Associated FibroblastsColorectal NeoplasmsExosomesMicroRNAsAnimalsCell Line, TumorCell ProliferationChemokine CXCL12Gene Expression Regulation, NeoplasticHumansMiceRepressor ProteinsChemokine CXCL12CXCL12 protein, humanMicroRNAsMIRN155 microRNA, humanMirn155 microRNA, mouseRepressor ProteinsZBTB2 protein, human

Identifiers

PMID35443745
PMCPMC9021302
OpenAlexW4224265938

What OpenQuestion holds

Textmetadata
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.