Evidence map›Paper›PMID 31348616›Full record

ArticleCancer medicine2019

Chemokine receptor 7 targets the vascular endothelial growth factor via the AKT/ERK pathway to regulate angiogenesis in colon cancer.

Xiang Li, Xuemei Wang, Zitao Li, Zhen Zhang, Yixia Zhang

Open access · goldAbstract read
In one paragraph

Article in Cancer medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.9field-weighted citation impact, top 12% 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

18 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
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  13. Review
  14. Advances in CXCR7 Modulators.Pharmaceuticals (Basel, Switzerland) · 2020
    Review
  15. Review
  16. CXCR7 Inhibits Fibrosis via Wnt/BioMed research international · 2020
    Article
  17. Article
  18. Article
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

5 authors at 2 institutions in 1 country.

Xiang LiDepartment of Ultrasonic Diagnosis, The First Affiliated Hospital, China Medical University, Shenyang, Liaoning, PR China.
Xuemei WangDepartment of Ultrasonic Diagnosis, The First Affiliated Hospital, China Medical University, Shenyang, Liaoning, PR China.ORCID https://orcid.org/0000-0002-4477-1865
Zitao LiDepartment of Orthopedic Surgery, Hongqi Hospital, Mudanjiang Medical University, Mudanjiang, Heilongjiang, PR China.
Zhen ZhangDepartment of Ultrasonic Diagnosis, The First Affiliated Hospital, China Medical University, Shenyang, Liaoning, PR China.
Yixia ZhangDepartment of Ultrasonic Diagnosis, The First Affiliated Hospital, China Medical University, Shenyang, Liaoning, PR China.
First Hospital of China Medical University · CNMudanjiang Medical University · CN

Funding

Liaoning Provincial Department of Education General Project L2013284
6 · The paper itself

Abstract

backgroundStudies have shown that CXCR7 is expressed in many tumors. The aim of the present study was to investigate the function of CXCR7 in colon cancer. Although evidence indicates that CXCR7 promotes angiogenesis in colon cancer, the mechanism involved in this process remains unclear.

methodsThe expression of CXCR7 in colon cancer was evaluated by quantitative reverse-transcription polymerase chain reaction and western blotting. After transfection, cell proliferation, migration, and lumen formation were measured in vitro. Immunohistochemistry and western blotting were used to identify the functional target of CXCR7 in vivo and in vitro.

resultsIn this study, CXCR7 was differentially expressed in four colon cancer cell lines. The proliferation and migration experiments showed that overexpression of CXCR7 enhanced cell growth and migration. Moreover, the tube formation assays showed that co-culture of colon cancer cells overexpressing CXCR7 with human umbilical vein endothelial cells significantly promoted tube formation in the latter cells. Conversely, the stable knockdown of CXCR7 significantly reduced this malignant activity. In addition, we found that CXCR7 activates the AKT and ERK pathways in colon cancer cells. The phosphorylation of AKT and ERK, as well as the expression of the vascular endothelial growth factor, can be inhibited using the LY294002 and U0126 inhibitors. Furthermore, the angiogenic ability of CXCR7-induced colon cancer cells was eliminated.

conclusionExpression of CXCR7 contributes to colon cancer growth and angiogenesis, by activating the AKT and ERK pathways. CXCR7 provides a potential therapeutic target against colon cancer.

Indexed as

Signal TransductionAnimalsCell Line, TumorCell MovementCell ProliferationColonic NeoplasmsDisease Models, AnimalExtracellular Signal-Regulated MAP KinasesFemaleGene ExpressionGene SilencingHeterograftsHumansMiceNeovascularization, PathologicProto-Oncogene Proteins c-aktACKR3 protein, humanExtracellular Signal-Regulated MAP KinasesProto-Oncogene Proteins c-aktReceptors, CXCRVascular Endothelial Growth Factor AVEGFA protein, humanAKTangiogenesiscolonCXCR7ERKvascular endothelial growth factor

Identifiers

PMID31348616
PMCPMC6718596
OpenAlexW2964728914

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Registered trials

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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.