Evidence map›Paper›PMID 22152097›Full record

ArticleJournal of translational medicine2011

Differentiation of breast cancer stem cells by knockdown of CD44: promising differentiation therapy.

Phuc V Pham, Nhan L C Phan, Nhung T Nguyen, Nhung H Truong, Thuy T Duong, Dong V Le, Kiet D Truong, Ngoc K Phan

Open access · goldAbstract read
In one paragraph

Article in Journal of translational medicine, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed, 1 pooled it
4.8field-weighted citation impact, top 4% 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

62 citing papers in PubMed, 1 synthesis or guideline pooled it, 128 citations in OpenAlex.

  1. Pooled it
  2. Fumiquinazolines F and G from the FungusInternational journal of molecular sciences · 2025
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  7. Growth dynamics of breast cancer stem cells: effects of self-feedback and EMT mechanisms.Theory in biosciences = Theorie in den Biowissenschaften · 2022
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2 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

8 authors at 3 institutions in 1 country.

Phuc V PhamLaboratory of Stem Cell Research and Application, University of Science, Vietnam National University, 227 Nguyen Van Cu, District 5, HCM City, Vietnam. pvphuc@hcmuns.edu.vn
Nhan L C Phan
Nhung T Nguyen
Nhung H Truong
Thuy T Duong
Dong V Le
Kiet D Truong
Ngoc K Phan
Vietnam National University Ho Chi Minh City · VNHo Chi Minh City University of Science · VNVietnam Military Medical University · VN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundBreast cancer stem cells (BCSCs) are the source of breast tumors. Compared with other cancer cells, cancer stem cells show high resistance to both chemotherapy and radiotherapy. Targeting of BCSCs is thus a potentially promising and effective strategy for breast cancer treatment. Differentiation therapy represents one type of cancer stem-cell-targeting therapy, aimed at attacking the stemness of cancer stem cells, thus reducing their chemo- and radioresistance. In a previous study, we showed that down-regulation of CD44 sensitized BCSCs to the anti-tumor agent doxorubicin. This study aimed to determine if CD44 knockdown caused BCSCs to differentiate into breast cancer non-stem cells (non-BCSCs).

methodsWe isolated a breast cancer cell population (CD44+CD24- cells) from primary cultures of malignant breast tumors. These cells were sorted into four sub-populations based on their expression of CD44 and CD24 surface markers. CD44 knockdown in the BCSC population was achieved using small hairpin RNA lentivirus particles. The differentiated status of CD44 knock-down BCSCs was evaluated on the basis of changes in CD44+CD24- phenotype, tumorigenesis in NOD/SCID mice, and gene expression in relation to renewal status, metastasis, and cell cycle in comparison with BCSCs and non-BCSCs.

resultsKnockdown of CD44 caused BCSCs to differentiate into non-BCSCs with lower tumorigenic potential, and altered the cell cycle and expression profiles of some stem cell-related genes, making them more similar to those seen in non-BCSCs.

conclusionsKnockdown of CD44 is an effective strategy for attacking the stemness of BCSCs, resulting in a loss of stemness and an increase in susceptibility to chemotherapy or radiation. The results of this study highlight a potential new strategy for breast cancer treatment through the targeting of BCSCs.

Indexed as

Cell DifferentiationGene Knockdown TechniquesAnimalsBreast NeoplasmsCD24 AntigenCell CycleCell ProliferationCell SeparationCell SurvivalCell Transformation, NeoplasticFemaleGene Expression Regulation, NeoplasticHumansHyaluronan ReceptorsMiceNeoplasm MetastasisCD24 AntigenHyaluronan ReceptorsRNA, Small Interfering

Identifiers

PMID22152097
PMCPMC3251542
OpenAlexW2139544398

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.