Evidence map›Paper›PMID 24809620›Full record

ArticleStem cells (Dayton, Ohio)2014

Chloroquine eliminates cancer stem cells through deregulation of Jak2 and DNMT1.

Dong Soon Choi, Elvin Blanco, Yoo-Shin Kim, Angel A Rodriguez, Hong Zhao, Tim Hui-Ming Huang, Chun-Liang Chen, Guangxu Jin, Melissa D Landis, Lacey A Burey and 7 more

Open access · bronzeAbstract read
In one paragraph

Article in Stem cells (Dayton, Ohio), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers.

0numbers the graph read from it
0cells of the map it votes in
71citing papers in PubMed
7.5field-weighted citation impact, top 2% 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

71 citing papers in PubMed, 117 citations in OpenAlex.

  1. Trial
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  12. Review
  13. Chloroquine and Chemotherapeutic Compounds in Experimental Cancer Treatment.International journal of molecular sciences · 2024
    Review
  14. Frontiers in pharmacology · 2024
    Article
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  20. Review

11 more citing papers are in PubMed but not listed here.

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

17 authors at 4 institutions in 1 country.

Dong Soon ChoiMethodist Cancer Center, Houston Methodist Hospital, Houston, Texas, USA.
Elvin Blanco
Yoo-Shin Kim
Angel A Rodriguez
Hong Zhao
Tim Hui-Ming Huang
Chun-Liang Chen
Guangxu Jin
Melissa D Landis
Lacey A Burey
Wei Qian
Sergio M Granados
Bhuvanesh Dave
Helen H Wong
Mauro Ferrari
Stephen T C Wong
Jenny C Chang
Methodist Hospital · USHouston Methodist · USThe University of Texas Health Science Center at San Antonio · USCornell University · US

Funding

The Core of the Computational BiologyU54CA149196 · NCI · METHODIST HOSPITAL RESEARCH INSTITUTE · PI WONG, STEPHEN TC · 2010 to 2015
$10.6M
Targeting Notch, PI3K-AKT and Other Novel Pathways in Breast Cancer Stem CellsR01CA138197 · NCI · METHODIST HOSPITAL RESEARCH INSTITUTE · PI CHANG, JENNY C-N, LEWIS, MICHAEL T. · 2008 to 2012
$2.3M
NCI NIH HHS R01 CA138197NCI NIH HHS U54 CA149196
6 · The paper itself

Abstract

Triple negative breast cancer (TNBC) is known to contain a high percentage of CD44(+) /CD24(-/low) cancer stem cells (CSCs), corresponding with a poor prognosis despite systemic chemotherapy. Chloroquine (CQ), an antimalarial drug, is a lysotropic reagent which inhibits autophagy. CQ was identified as a potential CSC inhibitor through in silico gene expression signature analysis of the CD44(+) /CD24(-/low) CSC population. Autophagy plays a critical role in adaptation to stress conditions in cancer cells, and is related with drug resistance and CSC maintenance. Thus, the objectives of this study were to examine the potential enhanced efficacy arising from addition of CQ to standard chemotherapy (paclitaxel) in TNBC and to identify the mechanism by which CQ eliminates CSCs in TNBCs. Herein, we report that CQ sensitizes TNBC cells to paclitaxel through inhibition of autophagy and reduces the CD44(+) /CD24(-/low) CSC population in both preclinical and clinical settings. Also, we are the first to report a mechanism by which CQ regulates the CSCs in TNBC through inhibition of the Janus-activated kinase 2 (Jak2)-signal transducer and activator of transcription 3 signaling pathway by reducing the expression of Jak2 and DNA methyltransferase 1.

Indexed as

AnimalsAutophagyCell Line, TumorChloroquineDNA (Cytosine-5-)-Methyltransferase 1DNA (Cytosine-5-)-MethyltransferasesFemaleHumansJanus Kinase 2MiceMice, NudeNeoplastic Stem CellsSignal TransductionTriple Negative Breast NeoplasmsChloroquineDNA (Cytosine-5-)-Methyltransferase 1DNA (Cytosine-5-)-MethyltransferasesDNMT1 protein, humanDnmt1 protein, mouseJAK2 protein, humanJanus Kinase 2AutophagyBreast cancer stem cellsChloroquineDNMT1Jak2

Identifiers

PMID24809620
PMCPMC4138251
OpenAlexW1915892937

What OpenQuestion holds

Textmetadata
LicenceTDM
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.