Evidence map›Paper›PMID 25114911›Full record

ArticleBioMed research international2014

Epigenetic silencing of CXCR4 promotes loss of cell adhesion in cervical cancer.

Suresh Singh Yadav, Shyam Babu Prasad, Mitali Das, Soni Kumari, Lakshmi Kant Pandey, Sunita Singh, Satyajit Pradhan, Gopeshwar Narayan

Open access · hybridAbstract read
In one paragraph

Article in BioMed research international, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.8field-weighted citation impact, top 14% 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

17 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
  2. Review
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  4. Article
  5. The Relaxin-3 Receptor, RXFP3, Is a Modulator of Aging-Related Disease.International journal of molecular sciences · 2022
    Review
  6. The Role of Chemokines in Cervical Cancers.Medicina (Kaunas, Lithuania) · 2021
    Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
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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

8 authors at 1 institution in 1 country.

Suresh Singh YadavDepartment of Molecular and Human Genetics, Banaras Hindu University, Varanasi 221005, India.ORCID 0000-0003-0309-8747
Shyam Babu PrasadDepartment of Molecular and Human Genetics, Banaras Hindu University, Varanasi 221005, India.
Mitali DasDepartment of Molecular and Human Genetics, Banaras Hindu University, Varanasi 221005, India.
Soni KumariDepartment of Molecular and Human Genetics, Banaras Hindu University, Varanasi 221005, India.
Lakshmi Kant PandeyDepartment of Obstetrics and Gynecology, Banaras Hindu University, Varanasi 221005, India.
Sunita SinghDepartment of Zoology, Mahila Mahavidyalaya, Banaras Hindu University, Varanasi 221005, India.
Satyajit PradhanDepartment of Radiotherapy & Radiation Medicine, Banaras Hindu University, Varanasi 221005, India.
Gopeshwar NarayanDepartment of Molecular and Human Genetics, Banaras Hindu University, Varanasi 221005, India.ORCID 0000-0001-5851-9997
Banaras Hindu University · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In the network of chemokine signaling pathways, recent reports have described the SDF-1α/CXCR4 axis and its role in cancer progression and metastasis. Interestingly, we found downregulation of CXCR4 at both transcript and protein level in cervical cancer cell lines and primary tumors. We also found CXCR4 promoter hypermethylation in cervical cancer cell lines and primary biopsy samples. DNA hypomethylating drug 5-AZA-2'-deoxycytidine and histone deacetylase inhibitor Trichostatin A treatments in cell lines reactivate both CXCR4 transcription and protein expression. Cell adhesion assay demonstrated that autocrine SDF-1α promotes the loss of cell adhesion while paracrine SDF-1α predominantly protects the normal cervical cells from loss of cell adhesion. Cervical cancer cell line C-33A having increased expression of CXCR4 after TSA treatment showed increased cell adhesion by paracrine source of SDF-1α in comparison to untreated C-33A. These findings demonstrate the first evidence that epigenetic silencing of CXCR4 makes the cells inefficient to respond to the paracrine source of SDF-1α leading to loss of cell adhesion, one of the key events in metastases and progression of the disease. Our results provide novel insight of SDF-1α/CXCR4 signaling in tumor microenvironment which may be promising to further delineate molecular mechanism of cervical carcinogenesis.

Indexed as

AdultAgedCell AdhesionCell Line, TumorCervix UteriChemokine CXCL12DNA MethylationFemaleGene SilencingHumansMiddle AgedReceptors, CXCR4Tumor MicroenvironmentUterine Cervical NeoplasmsChemokine CXCL12CXCR4 protein, humanReceptors, CXCR4

Identifiers

PMID25114911
PMCPMC4119908
OpenAlexW2098352775

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.