Evidence map›Paper›PMID 36210463›Full record

ArticleCell & bioscience2022

CXCL12/CXCR7/β-arrestin1 biased signal promotes epithelial-to-mesenchymal transition of colorectal cancer by repressing miRNAs through YAP1 nuclear translocation.

Mahan Si, Yujia Song, Xiaohui Wang, Dong Wang, Xiaohui Liu, Xianjun Qu, Zhiyu Song, Xinfeng Yu

Open access · goldAbstract read
In one paragraph

Article in Cell & bioscience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing 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

11 citing papers in PubMed, 18 citations in OpenAlex.

  1. Review
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  9. Regulation of the Hippo/YAP axis by CXCR7 in the tumorigenesis of gastric cancer.Journal of experimental & clinical cancer research : CR · 2023
    Article
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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 2 institutions in 1 country.

Mahan SiDepartment of Pharmacology, School of Basic Medical Sciences, Capital Medical University, Beijing, China.
Yujia SongDepartment of Pharmacology, School of Basic Medical Sciences, Capital Medical University, Beijing, China.
Xiaohui WangDepartment of General Surgery, Xuanwu Hospital, Capital Medical University, Beijing, China.
Dong WangDepartment 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.
Xianjun QuDepartment of Pharmacology, School of Basic Medical Sciences, Capital Medical University, Beijing, China.
Zhiyu SongDepartment of Pharmacy, Henan Provincial People's Hospital, People's Hospital of Zhengzhou University, Zhengzhou, Henan, China.
Xinfeng YuDepartment of Pharmacology, School of Basic Medical Sciences, Capital Medical University, Beijing, China. xyu@ccmu.edu.cn.
Capital Medical University · CNHenan Provincial People's Hospital · CN

Funding

National Natural Science Foundation of China 81872884National Natural Science Foundation of China 82002574National Natural Science Foundation of China 82073876Natural Science Foundation of Beijing Municipality 7202012
6 · The paper itself

Abstract

backgroundChemokine CXC motif receptor 7 (CXCR7) is an atypical G protein-coupled receptor (GPCR) that signals in a biased fashion. CXCL12/CXCR7 biased signal has been reported to play crucial roles in multiple stages of colorectal cancer (CRC). However, the mechanism of CXCL12/CXCR7 biased signal in promoting CRC progression and metastasis remains obscure.

resultsWe demonstrate that CXCR7 activation promotes EMT and upregulates the expression of Vimentin and doublecortin-like kinase 1 (DCLK1) in CRC cells with concurrent repression of miR-124-3p and miR-188-5p through YAP1 nuclear translocation. Cell transfection and luciferase assay prove that these miRNAs regulate EMT by targeting Vimentin and DCLK1. More importantly, CXCL12/CXCR7/β-arrestin1-mediated biased signal induces YAP1 nuclear translocation, which functions as a transcriptional repressor by interacting with Yin Yang 1 (YY1) and recruiting YY1 to the promoters of miR-124-3p and miR-188-5p. Pharmacological inhibitor of YAP1 suppresses EMT and tumor metastasis upon CXCR7 activation in vivo in tumor xenografts of nude mice and inflammatory colonic adenocarcinoma models. Clinically, the expression of CXCR7 is positively correlated with nuclear YAP1 levels and EMT markers.

conclusionsOur studies reveal a novel mechanism and clinical significance of CXCL12/CXCR7 biased signal in promoting EMT and invasion in CRC progression. These findings highlight the potential of targeting YAP1 nuclear translocation in hampering CXCL12/CXCR7 biased signal-induced metastasis of colorectal cancer.

Indexed as

Biased signalColorectal cancerCXCR7Epithelial-to-mesenchymal transitionmiRNAsYAP1

Identifiers

PMID36210463
PMCPMC9549625
OpenAlexW4303940404

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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.