Evidence map›Paper›PMID 33335962›Full record

ArticleGenes & diseases2020

ROS and Lipid Droplet accumulation induced by high glucose exposure in healthy colon and Colorectal Cancer Stem Cells.

Luca Tirinato, Francesca Pagliari, Simone Di Franco, Elisa Sogne, Maria Grazia Marafioti, Jeanette Jansen, Andrea Falqui, Matilde Todaro, Patrizio Candeloro, Carlo Liberale and 3 more

Open access · diamondAbstract read
In one paragraph

Article in Genes & diseases, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
3.1field-weighted citation impact, top 9% 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

21 citing papers in PubMed, 41 citations in OpenAlex.

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  16. Mechanistic roles of mutant p53 governing lipid metabolism.Advances in biological regulation · 2022
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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

13 authors at 4 institutions in 3 countries.

Luca TirinatoBiomedical Physics in Radiation Oncology, DKFZ (German Cancer Research Center), 69120 Heidelberg, Germany.
Francesca PagliariBiomedical Physics in Radiation Oncology, DKFZ (German Cancer Research Center), 69120 Heidelberg, Germany.
Simone Di FrancoCellular and Molecular Pathophysiology Laboratory, Department of Surgical, Oncological and Stomatological Sciences, University of Palermo, Palermo, Italy.
Elisa SogneBiological and Environmental Sciences and Engineering (BESE) Division, King Abdullah University of Science and Technology (KAUST), Thuwal 23955-6900, Saudi Arabia.
Maria Grazia MarafiotiBiomedical Physics in Radiation Oncology, DKFZ (German Cancer Research Center), 69120 Heidelberg, Germany.
Jeanette JansenBiomedical Physics in Radiation Oncology, DKFZ (German Cancer Research Center), 69120 Heidelberg, Germany.
Andrea FalquiBiological and Environmental Sciences and Engineering (BESE) Division, King Abdullah University of Science and Technology (KAUST), Thuwal 23955-6900, Saudi Arabia.
Matilde TodaroDepartment of Health Promotion, Mother and Child Care, Internal Medicine and Medical Specialties (PROMISE), University of Palermo, Palermo, Italy.
Patrizio CandeloroDepartment of Experimental and Clinical Medicine, University "Magna Graecia" of Catanzaro, 88100 Loc. Germaneto, Catanzaro, Italy.
Carlo LiberaleBiological and Environmental Sciences and Engineering (BESE) Division, King Abdullah University of Science and Technology (KAUST), Thuwal 23955-6900, Saudi Arabia.
Joao SecoBiomedical Physics in Radiation Oncology, DKFZ (German Cancer Research Center), 69120 Heidelberg, Germany.
Giorgio StassiCellular and Molecular Pathophysiology Laboratory, Department of Surgical, Oncological and Stomatological Sciences, University of Palermo, Palermo, Italy.
Enzo Di FabrizioPhysical Science and Engineering (PSE) Division, King Abdullah University of Science and Technology (KAUST), Thuwal, Saudi Arabia.
German Cancer Research Center · DEKing Abdullah University of Science and Technology · SAUniversity of Palermo · ITMagna Graecia University · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lipid Droplets (LDs) are emerging as crucial players in colon cancer development and maintenance. Their expression has been associated with high tumorigenicity in Cancer Stem Cells (CSCs), so that they have been proposed as a new functional marker in Colorectal Cancer Stem Cells (CR-CSCs). They are also indirectly involved in the modulation of the tumor microenvironment through the production of pro-inflammatory molecules. There is growing evidence that a possible connection between metabolic alterations and malignant transformation exists, although the effects of nutrients, primarily glucose, on the CSC behavior are still mostly unexplored. Glucose is an essential fuel for cancer cells, and the connections with LDs in the healthy and CSC populations merit to be more deeply investigated. Here, we showed that a high glucose concentration activated the PI3K/AKT pathway and increased the expression of CD133 and CD44v6 CSC markers. Additionally, glucose was responsible for the increased amount of Reactive Oxygen Species (ROS) and LDs in both healthy and CR-CSC samples. We also investigated the gene modulations following the HG treatment and found out that the healthy cell gene profile was the most affected. Lastly, Atorvastatin, a lipid-lowering drug, induced the highest mortality on CR-CSCs without affecting the healthy counterpart.

Indexed as

Cholesterol metabolismColorectal cancer stem cellsFatty acid metabolismHigh glucoseLipid dropletsOncogenesOxidative stressPI3K-AKT

Identifiers

PMID33335962
PMCPMC7729111
OpenAlexW2976836496

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.