Evidence map›Paper›PMID 17046751›Full record

ArticleExperimental cell research2006

Endonuclease G promotes cell death of non-invasive human breast cancer cells.

Alexei G Basnakian, Eugene O Apostolov, Xiaoyan Yin, Stanley O Abiri, Anna G Stewart, Amar B Singh, Sudhir V Shah

Open access · greenAbstract read
In one paragraph

Article in Experimental cell research, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.4field-weighted citation impact, top 22% 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

22 citing papers in PubMed, 53 citations in OpenAlex.

  1. Article
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  9. Article
  10. Anti-ROR1 scFv-EndoG as a Novel Anti-Cancer Therapeutic DrugAsian Pacific journal of cancer prevention : APJCP · 2018
    Article
  11. Article
  12. Article
  13. Killing of cancer cells through the use of eukaryotic expression vectors harbouring genes encoding nucleases and ribonuclease inhibitor.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015
    Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Endonuclease G mediates endothelial cell death induced by carbamylated LDL.American journal of physiology. Heart and circulatory physiology · 2011
    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 3 institutions in 1 country.

Alexei G BasnakianDivision of Nephrology, Department of Internal Medicine, University of Arkansas for Medical Sciences, slot #501, 4301 W. Markham St., Little Rock, AR 72205, USA. basnakianalexeig@uams.edu
Eugene O Apostolov
Xiaoyan Yin
Stanley O Abiri
Anna G Stewart
Amar B Singh
Sudhir V Shah
University of Arkansas for Medical Sciences · USCentral Arkansas Veterans Healthcare System · USPhilander Smith College · US

Funding

The Role of MAPKs in Renal Epithelial Cell SurvivalP01DK058324 · NIDDK · UNIVERSITY OF ARKANSAS MED SCIS LTL ROCK · PI SHAH, SUDHIR V · 2001 to 2005
$4.4M
Endonuclease dificiency in breast cancer progressionR03CA114729 · NCI · UNIV OF ARKANSAS FOR MED SCIS · PI BASNAKIAN, ALEXEI G · 2005 to 2006
$125k
Nuclease mechanisms in acute kidney injuryI01BX002425 · VA · CENTRAL ARKANSAS VETERANS HLTHCARE SYS · PI Alexei G Basnakian · 2015 to 2026
–
BLRD VA I01 BX002425NCI NIH HHS 5R03CA114729-02NCI NIH HHS R03 CA114729NIDDK NIH HHS 5P01DK58324-04NIDDK NIH HHS P01 DK058324
6 · The paper itself

Abstract

The invasiveness of breast cancer cells was shown to be associated with the suppressed ability to develop apoptosis. The role of cell death DNases/endonucleases has not been previously examined in relation with the invasiveness of breast cancer cells. We have compared the activity of the endonucleases in seven human breast cancer cell lines different in the level of invasiveness and differentiation. The invasiveness of cell lines was confirmed by an in vitro Matrigel-based assay. The total endonuclease activity in the differentiated non-invasive (WDNI) cell lines was higher than that in the poorly differentiated invasive (PDI) cells. The expression of EndoG strongly correlated with the degree of estrogen receptor expression and showed an inverse correlation with vimentin and matrix metalloproteinase-13. The EndoG-positive WDNI cells were more sensitive to etoposide- or camptothecin-induced cell death than EndoG-negative PDI cells. Silencing of EndoG caused inhibited of SK-BR-3 WDNI cell death induced by etoposide. Human ductal carcinomas in situ expressed high levels of EndoG, while invasive medullar and ductal carcinomas had significantly decreased expression of EndoG. This correlated with decreased apoptosis as measured by TUNEL assay. Our findings suggest that the presence of EndoG in non-invasive breast cancer cells determines their sensitivity to apoptosis, which may be taken into consideration for developing the chemotherapeutic strategy for cancer treatment.

Indexed as

ApoptosisCell MovementAnimalsBreastBreast NeoplasmsCamptothecinCell DeathCell Line, TumorDNA FragmentationEndodeoxyribonucleasesEtoposideHumansMiceMice, KnockoutTransfectionCamptothecinEndodeoxyribonucleasesendonuclease GEtoposide

Identifiers

PMID17046751
PMCPMC1839947
OpenAlexW1993955706

What OpenQuestion holds

Textmetadata
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.