Evidence map›Paper›PMID 27680705›Full record

ArticleNature2016

The lipolysis pathway sustains normal and transformed stem cells in adult Drosophila.

Shree Ram Singh, Xiankun Zeng, Jiangsha Zhao, Ying Liu, Gerald Hou, Hanhan Liu, Steven X Hou

Abstract read
In one paragraph

Article in Nature, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
–field-weighted citation impact
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

54 citing papers in PubMed.

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  9. Novel Arf1 Inhibitors Drive Cancer Stem Cell Aging and Potentiate Anti-Tumor Immunity.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024
    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

7 authors.

Shree Ram SinghThe Basic Research Laboratory, National Cancer Institute at Frederick, National Institutes of Health, Frederick, Maryland 21702, USA.
Xiankun ZengThe Basic Research Laboratory, National Cancer Institute at Frederick, National Institutes of Health, Frederick, Maryland 21702, USA.
Jiangsha ZhaoThe Basic Research Laboratory, National Cancer Institute at Frederick, National Institutes of Health, Frederick, Maryland 21702, USA.
Ying LiuThe Basic Research Laboratory, National Cancer Institute at Frederick, National Institutes of Health, Frederick, Maryland 21702, USA.
Gerald HouThe Basic Research Laboratory, National Cancer Institute at Frederick, National Institutes of Health, Frederick, Maryland 21702, USA.
Hanhan LiuThe Basic Research Laboratory, National Cancer Institute at Frederick, National Institutes of Health, Frederick, Maryland 21702, USA.
Steven X HouThe Basic Research Laboratory, National Cancer Institute at Frederick, National Institutes of Health, Frederick, Maryland 21702, USA.

Funding

Molecular Genetic Study of Stem Cells, Cancer Stem Cells, and Stem Cell AgingZIABC010738 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI HOU, STEVEN · 2009 to 2020
$14.4M
Molecular Genetic Study of Stem Cells, Cancer Stem Cells, and Stem Cell AgingZ01BC010738 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI HOU, XIANYU S · 2006 to 2008
$2.7M
Intramural NIH HHS Z01 BC010738
6 · The paper itself

Abstract

Cancer stem cells (CSCs) may be responsible for tumour dormancy, relapse and the eventual death of most cancer patients. In addition, these cells are usually resistant to cytotoxic conditions. However, very little is known about the biology behind this resistance to therapeutics. Here we investigated stem-cell death in the digestive system of adult Drosophila melanogaster. We found that knockdown of the coat protein complex I (COPI)-Arf79F (also known as Arf1) complex selectively killed normal and transformed stem cells through necrosis, by attenuating the lipolysis pathway, but spared differentiated cells. The dying stem cells were engulfed by neighbouring differentiated cells through a draper-myoblast city-Rac1-basket (also known as JNK)-dependent autophagy pathway. Furthermore, Arf1 inhibitors reduced CSCs in human cancer cell lines. Thus, normal or cancer stem cells may rely primarily on lipid reserves for energy, in such a way that blocking lipolysis starves them to death. This finding may lead to new therapies that could help to eliminate CSCs in human cancers.

Indexed as

ADP-Ribosylation Factor 1AnimalsApoptosisAutophagyCell DifferentiationCell Line, TumorCell ProliferationCell SurvivalCell Transformation, NeoplasticCoat Protein Complex IDrosophila melanogasterDrosophila ProteinsDrug Resistance, NeoplasmEnergy MetabolismEnterocytesFemaleADP-Ribosylation Factor 1Coat Protein Complex IDrosophila Proteinsdrpr protein, DrosophilaJNK Mitogen-Activated Protein KinasesMembrane Proteinsrac GTP-Binding Proteins

Identifiers

PMID27680705
PMCPMC7798135

What OpenQuestion holds

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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.