CXCL5: A coachman to drive cancer progression
Frontiers in Oncology, ISSN: 2234-943X, Vol: 12, Page: 944494
2022
- 36Citations
- 42Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
Citation Benchmarking is provided by Scopus and SciVal and is different from the metrics context provided by PlumX Metrics.
Metrics Details
- Citations36
- Citation Indexes36
- 36
- Captures42
- Readers42
- 42
Review Description
Chemokines are a class of pro-inflammatory cytokines that can recruit and activate chemotactic cells. C‐X‐C motif chemokine ligand 5 (CXCL5) is a member of the chemokine family binding CXCR2 (C-X-C Motif Chemokine Receptor 2), a G-protein coupled receptor. Accumulated evidence has shown that dysregulated CXCL5 participates in tumor metastasis and angiogenesis in human malignant tumors. In this review, we summarized the advances in research on CXCL5, including its dysregulation in different tumors and the mechanism associated with tumor behavior (formation of the immunosuppressive microenvironment, promotion of tumor angiogenesis, and metastasis). We also summarized and discussed the perspective about the potential application of CXCL5 in tumor therapy targeting the tumor inflammatory microenvironment.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=85136163861&origin=inward; http://dx.doi.org/10.3389/fonc.2022.944494; http://www.ncbi.nlm.nih.gov/pubmed/35978824; https://www.frontiersin.org/articles/10.3389/fonc.2022.944494/full; https://dx.doi.org/10.3389/fonc.2022.944494; https://www.frontiersin.org/journals/oncology/articles/10.3389/fonc.2022.944494/full
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