Evidence map›Paper›PMID 26421710›Full record

ArticleOncotarget2015

High mitochondrial mass identifies a sub-population of stem-like cancer cells that are chemo-resistant.

Gillian Farnie, Federica Sotgia, Michael P Lisanti

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 121 papers.

0numbers the graph read from it
0cells of the map it votes in
121citing papers in PubMed
8.8field-weighted citation impact, top 1% 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

121 citing papers in PubMed, 194 citations in OpenAlex.

  1. Article
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  4. The metabolic profiles of cancer stem cells.Stem cell research & therapy · 2026
    Review
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  18. Breast Cancer Chemoresistance: Insights into the Regulatory Role of lncRNA.International journal of molecular sciences · 2023
    Review
  19. Article
  20. Review

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors at 2 institutions in 1 country.

Gillian FarnieCancer Stem Cell Research, Institute of Cancer Sciences, University of Manchester, Manchester, UK.
Federica SotgiaThe Breast Cancer Now Research Unit, Institute of Cancer Sciences, University of Manchester, Manchester, UK.
Michael P LisantiThe Breast Cancer Now Research Unit, Institute of Cancer Sciences, University of Manchester, Manchester, UK.
University of Manchester · GBCancer Research UK Manchester Institute · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chemo-resistance is a clinical barrier to more effective anti-cancer therapy. In this context, cancer stem-like cells (CSCs) are thought to be chemo-resistant, resulting in tumor recurrence and distant metastasis. Our hypothesis is that chemo-resistance in CSCs is driven, in part, by enhanced mitochondrial function. Here, we used breast cell lines and metastatic breast cancer patient samples to begin to dissect the role of mitochondrial metabolism in conferring the CSC phenotype. More specifically, we employed fluorescent staining with MitoTracker (MT) to metabolically fractionate these cell lines into mito-high and mito-low sub-populations, by flow-cytometry. Interestingly, cells with high mitochondrial mass (mito-high) were specifically enriched in a number of known CSC markers, such as aldehyde dehydrogenase (ALDH) activity, and they were ESA+/CD24-/low and formed mammospheres with higher efficiency. Large cell size is another independent characteristic of the stem cell phenotype; here, we observed a >2-fold increase in mitochondrial mass in large cells (>12-μm), relative to the smaller cell population (4-8-μm). Moreover, the mito-high cell population showed a 2.4-fold enrichment in tumor-initiating cell activity, based on limiting dilution assays in murine xenografts. Importantly, primary human breast CSCs isolated from patients with metastatic breast cancer or a patient derived xenograft (PDX) also showed the co-enrichment of ALDH activity and mitochondrial mass. Most significantly, our investigations demonstrated that mito-high cells were resistant to paclitaxel, resulting in little or no DNA damage, as measured using the comet assay. In summary, increased mitochondrial mass in a sub-population of breast cancer cells confers a stem-like phenotype and chemo-resistance. As such, our current findings have important clinical implications for over-coming drug resistance, by therapeutically targeting the mito-high CSC population.

Indexed as

Aldehyde DehydrogenaseAnimalsAntigens, NeoplasmAntineoplastic Agents, PhytogenicBreast NeoplasmsCD24 AntigenCell Adhesion MoleculesComet AssayDNA DamageDrug Resistance, NeoplasmEpithelial Cell Adhesion MoleculeFemaleFlow CytometryHumansMCF-7 CellsMiceAldehyde DehydrogenaseAntigens, NeoplasmAntineoplastic Agents, PhytogenicCD24 AntigenCD24 protein, humanCell Adhesion MoleculesEpithelial Cell Adhesion MoleculePaclitaxelcancer stem cellsmitochondriaMitoTrackertumor metabolism

Identifiers

PMID26421710
PMCPMC4741545
OpenAlexW2136679767

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.