Evidence map›Paper›PMID 33466690›Full record

ArticleGenes2021

Inhibition of the Lipid Droplet-Peroxisome Proliferator-Activated Receptor α Axis Suppresses Cancer Stem Cell Properties.

Kenta Kuramoto, Masahiro Yamamoto, Shuhei Suzuki, Keita Togashi, Tomomi Sanomachi, Chifumi Kitanaka, Masashi Okada

Open access · goldAbstract read
In one paragraph

Article in Genes, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

28 citing papers in PubMed, 31 citations in OpenAlex.

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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 at 1 institution in 1 country.

Kenta KuramotoDepartment of Molecular Cancer Science, Yamagata University School of Medicine, Yamagata 990-9585, Japan.
Masahiro YamamotoDepartment of Molecular Cancer Science, Yamagata University School of Medicine, Yamagata 990-9585, Japan.ORCID 0000-0002-0652-6105
Shuhei SuzukiDepartment of Molecular Cancer Science, Yamagata University School of Medicine, Yamagata 990-9585, Japan.
Keita TogashiDepartment of Molecular Cancer Science, Yamagata University School of Medicine, Yamagata 990-9585, Japan.
Tomomi SanomachiDepartment of Molecular Cancer Science, Yamagata University School of Medicine, Yamagata 990-9585, Japan.
Chifumi KitanakaDepartment of Molecular Cancer Science, Yamagata University School of Medicine, Yamagata 990-9585, Japan.
Masashi OkadaDepartment of Molecular Cancer Science, Yamagata University School of Medicine, Yamagata 990-9585, Japan.
Yamagata University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancer stem cells (CSCs), having both self-renewal and tumorigenic capacity, utilize an energy metabolism system different from that of non-CSCs. Lipid droplets (LDs) are organelles that store neutral lipids, including triacylglycerol. Previous studies demonstrated that LDs are formed and store lipids as an energy source in some CSCs. LDs play central roles not only in lipid storage, but also as a source of endogenous lipid ligands, which are involved in numerous signaling pathways, including the peroxisome proliferator-activated receptor (PPAR) signaling pathway. However, it remains unclear whether LD-derived signal transduction is involved in the maintenance of the properties of CSCs. We investigated the roles of LDs in cancer stemness using pancreatic and colorectal CSCs and isogenic non-CSCs. PPARα was activated in CSCs in which LDs accumulated, but not in non-CSCs, and pharmacological and genetic inhibition of PPARα suppressed cancer stemness. In addition, inhibition of both re-esterification and lipolysis pathways suppressed cancer stemness. Our study suggested that LD metabolic turnover accompanying PPARα activation is a promising anti-CSC therapeutic target.

Indexed as

Colorectal NeoplasmsEnergy MetabolismHT29 CellsHumansLipid DropletsNeoplasm ProteinsNeoplastic Stem CellsPancreatic NeoplasmsPPAR alphaSignal TransductionNeoplasm ProteinsPPAR alphaPPARA protein, humancancer-initiating cellcolorectal cancerlipid dropletlipolysispancreatic cancerperoxisome proliferator-activated receptorre-esterification

Identifiers

PMID33466690
PMCPMC7828779
OpenAlexW3120525871

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.