Evidence map›Paper›PMID 36268282›Full record

ReviewJournal of oncology2022

Chemokine/GPCR Signaling-Mediated EMT in Cancer Metastasis.

Xutengyue Tian, Jiayi Wang, Lanxin Jiang, Yuchen Jiang, Juan Xu, Xiaodong Feng

Open access · hybridAbstract readReview
In one paragraph

Review in Journal of oncology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.4field-weighted citation impact, top 17% 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

12 citing papers in PubMed, 14 citations in OpenAlex.

  1. Review
  2. Suppression of NGALR impedes TNBC cell survival, proliferation, invasion, and migration through Akt/mTOR and JAK/STAT3 pathway inhibition.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
    Article
  3. Review
  4. Review
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Pharmacological reviews · 2023
    Review
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

6 authors at 1 institution in 1 country.

Xutengyue TianState Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, Research Unit of Oral Carcinogenesis and Management, Chinese Academy of Medical Sciences, West China Hospital of Stomatology, Sichuan University, Chengdu, Sichuan 610041, China.ORCID https://orcid.org/0000-0002-8526-2661
Jiayi WangState Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, Research Unit of Oral Carcinogenesis and Management, Chinese Academy of Medical Sciences, West China Hospital of Stomatology, Sichuan University, Chengdu, Sichuan 610041, China.
Lanxin JiangState Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, Research Unit of Oral Carcinogenesis and Management, Chinese Academy of Medical Sciences, West China Hospital of Stomatology, Sichuan University, Chengdu, Sichuan 610041, China.
Yuchen JiangState Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, Research Unit of Oral Carcinogenesis and Management, Chinese Academy of Medical Sciences, West China Hospital of Stomatology, Sichuan University, Chengdu, Sichuan 610041, China.ORCID https://orcid.org/0000-0003-0968-2012
Juan XuDepartment of Stomatology, Sijing Hospital, Shanghai 210061, China.ORCID https://orcid.org/0000-0001-7931-3146
Xiaodong FengState Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, Research Unit of Oral Carcinogenesis and Management, Chinese Academy of Medical Sciences, West China Hospital of Stomatology, Sichuan University, Chengdu, Sichuan 610041, China.ORCID https://orcid.org/0000-0002-2741-5420
Chinese Academy of Medical Sciences & Peking Union Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Metastasis, the chief cause of cancer-related deaths, is associated with epithelial-mesenchymal transition (EMT). In the tumor microenvironment, EMT can be triggered by chemokine/G-protein-coupled receptor (GPCR) signaling, which is closely associated with tumor progression. However, the functional links between chemokine/GPCR signaling-mediated EMT and metastasis remain unclear. Herein, we summarized the mechanisms of chemokine/GPCR signaling-mediated EMT with an insight into facilitating metastasis and clarified the role of chemokine in the local invasion, intravasation, circulation, extravasation, and colonization, respectively. Moreover, several potential pathways that might contribute to EMT based on the latest studies on GPCR signaling were proposed, including signaling mediated by G protein,

Identifiers

PMID36268282
PMCPMC9578795
OpenAlexW4304588376

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.