Evidence map›Paper›PMID 30804329›Full record

ArticleCell death & disease2019

CXCR7 promotes melanoma tumorigenesis via Src kinase signaling.

Siran Xu, Jiaze Tang, Chunying Wang, Jie Liu, Yan Fu, Yongzhang Luo

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.5field-weighted citation impact, top 16% 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

20 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
  2. Review
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  6. Pharmacological reviews · 2023
    Review
  7. Review
  8. Review
  9. CXCL12-CXCR4/CXCR7 Axis in Cancer: from Mechanisms to Clinical Applications.International journal of biological sciences · 2023
    Review
  10. Review
  11. Review
  12. Crosstalk between CXCR4/ACKR3 and EGFR Signaling in Breast Cancer Cells.International journal of molecular sciences · 2022
    Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Review
  20. 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 2 institutions in 1 country.

Siran XuPeking University-Tsinghua University-National Institute of Biological Sciences Joint Graduate Program (PTN), School of Life Sciences, Peking University, Beijing, China.
Jiaze TangThe National Engineering Laboratory for Anti-Tumor Protein Therapeutics, Tsinghua University, Beijing, China.
Chunying WangThe National Engineering Laboratory for Anti-Tumor Protein Therapeutics, Tsinghua University, Beijing, China.
Jie LiuThe National Engineering Laboratory for Anti-Tumor Protein Therapeutics, Tsinghua University, Beijing, China.
Yan FuThe National Engineering Laboratory for Anti-Tumor Protein Therapeutics, Tsinghua University, Beijing, China.
Yongzhang LuoThe National Engineering Laboratory for Anti-Tumor Protein Therapeutics, Tsinghua University, Beijing, China. yluo@mail.tsinghua.edu.cn.
Tsinghua University · CNPeking University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chemokine receptors have been documented to exert critical functions in melanoma progression. However, current drugs targeting these receptors have limited efficacy in clinical applications, suggesting the urgency to further explore the roles of chemokine receptors in melanoma. Here we found that C-X-C chemokine receptor 7 (CXCR7) was the most highly expressed chemokine receptor in murine melanoma cell lines. In addition, the expression level of CXCR7 was positively correlated with melanoma progression in the clinical samples. High CXCR7 expression was associated with shorter overall survival in melanoma patients. Increased expression of CXCR7 augmented melanoma proliferation in vitro and tumor growth in vivo, whereas knockout of CXCR7 exhibited significant inhibitory effects. Moreover, our data elucidated that CXCR7 activated Src kinase phosphorylation in a β-arrestin2-dependent manner. The administration of the Src kinase inhibitor PP1 or siRNA specific for β-arrestin2 abolished CXCR7-promoted cell proliferation. Importantly, CXCR7 also regulated melanoma angiogenesis and the secretion of vascular endothelial growth factor (VEGF). Subsequent investigations revealed a novel event that the activation of the CXCR7-Src axis stimulated the phosphorylation of eukaryotic translation initiation factor 4E (eIF4E) to accelerate the translation of hypoxia-inducible factor 1α (HIF-1α), which enhanced the secretion of VEGF from melanoma cells. Collectively, our results illuminate the crucial roles of CXCR7 in melanoma tumorigenesis, and indicate the potential of targeting CXCR7 as new therapeutic strategies for melanoma treatment.

Indexed as

Signal TransductionA549 CellsAdolescentAdultAgedAged, 80 and overAnimalsbeta-Arrestin 2CarcinogenesisCell ProliferationCell Transformation, NeoplasticChildChild, PreschoolEukaryotic Initiation Factor-4EFemaleHEK293 CellsACKR3 protein, humanbeta-Arrestin 2Cmkor1 protein, mouseEukaryotic Initiation Factor-4EHif1a protein, mouseHypoxia-Inducible Factor 1, alpha SubunitReceptors, CXCRsrc-Family KinasesVascular Endothelial Growth Factor A

Identifiers

PMID30804329
PMCPMC6389959
OpenAlexW2917666000

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.