Evidence map›Paper›PMID 24915301›Full record

ArticlePloS one2014

Inhibition of chemokine (C-C motif) receptor 7 sialylation suppresses CCL19-stimulated proliferation, invasion and anti-anoikis.

Mei-Lin Su, Tsung-Ming Chang, Chi-Hsiang Chiang, Han-Chen Chang, Ming-Feng Hou, Wen-Shan Li, Wen-Chun Hung

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.7field-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

23 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Does CCL19 act as a double-edged sword in cancer development?Clinical and experimental immunology · 2022
    Review
  9. Review
  10. Article
  11. Review
  12. Article
  13. Review
  14. Cosmc controls B cell homing.Nature communications · 2020
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

7 authors at 4 institutions in 1 country.

Mei-Lin SuInstitute of Biomedical Sciences, National Sun Yat-Sen University, Kaohsiung, Taiwan, Republic of China.
Tsung-Ming ChangNational Institute of Cancer Research, National Health Research Institutes, Tainan, Taiwan, Republic of China.
Chi-Hsiang ChiangNational Institute of Cancer Research, National Health Research Institutes, Tainan, Taiwan, Republic of China.
Han-Chen ChangInstitute of Chemistry, Academia Sinica, Taipei, Taiwan, Republic of China.
Ming-Feng HouDepartment of Surgery, College of Medicine, Kaohsiung Medical University, and Department of Surgery, Kaohsiung Municipal Ta-Tung Hospital, Kaohsiung, Taiwan, Republic of China; Cancer Center, Kaohsiung Medical University Hospital, Kaohsiung, Taiwan, Republic of China.
Wen-Shan LiInstitute of Chemistry, Academia Sinica, Taipei, Taiwan, Republic of China.
Wen-Chun HungInstitute of Biomedical Sciences, National Sun Yat-Sen University, Kaohsiung, Taiwan, Republic of China; National Institute of Cancer Research, National Health Research Institutes, Tainan, Taiwan, Republic of China.
Institute of Chemistry, Academia Sinica · TWNational Health Research Institutes · TWNational Sun Yat-sen University · TWKaohsiung Medical University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chemokine (C-C motif) receptor 7 (CCR7) is involved in lymph-node homing of naive and regulatory T cells and lymphatic metastasis of cancer cells. Sialic acids comprise a group of monosaccharide units that are added to the terminal position of the oligosaccharide chain of glycoproteins by sialyation. Recent studies suggest that aberrant sialylation of receptor proteins contributes to proliferation, motility, and drug resistance of cancer cells. In this study, we addressed whether CCR7 is a sialylated receptor protein and tried to elucidate the effect of sialylation in the regulation of signal transduction and biological function of CCR7. Our results demonstrated that α-2, 3-sialyltransferase which catalyze sialylation reaction in vivo was overexpressed in breast tumor tissues and cell lines. Lectin blot analysis clearly demonstrated that CCR7 receptor was sialyated in breast cancer cells. Chemokine (C-C motif) ligand 19 (CCL19), the cognate ligand for CCR7, induced the activation of extracellular signal-regulated kinase (ERK) and AKT signaling and increased the expression of cell cycle regulatory proteins and proliferation of breast cancer cells. When cells were pre-treated with a sialyltransferase inhibitor AL10 or sialidase, CCL19-induced cell growth was significantly suppressed. CCL19 also increased invasion and prevented anoikis by up-regulating pro-survival proteins Bcl-2 and Bcl-xL. Inhibition of sialylation by AL10 totally abolished these effects. Finally, we showed that AL10 inhibited tumorigenicity of breast cancer in experimental animals. Taken together, we demonstrate for the first time that CCR7 receptor is a sialylated protein and sialylation is important for the paracrine stimulation by its endogenous ligand CCL19. In addition, inhibition of aberrant sialylation of CCR7 suppresses proliferation and invasion and triggers anoikis in breast cancer cells. Targeting of sialylation enzymes may be a novel strategy for breast cancer treatment.

Indexed as

AnoikisAnimalsbeta-Galactoside alpha-2,3-SialyltransferaseBreast NeoplasmsCell LineCell MovementCell ProliferationCell Transformation, NeoplasticChemokine CCL19Cyclin D1Disease Models, AnimalEpithelial CellsFemaleGene ExpressionGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betabeta-Galactoside alpha-2,3-SialyltransferaseChemokine CCL19Cyclin D1Glycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaReceptors, CCR7SialyltransferasesST3GAL1 protein, human

Identifiers

PMID24915301
PMCPMC4051673
OpenAlexW2023475375

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.