Evidence map›Paper›PMID 34771647›Full record

ReviewCancers2021

Lipid Catabolism and ROS in Cancer: A Bidirectional Liaison.

Serena Castelli, Pamela De Falco, Fabio Ciccarone, Enrico Desideri, Maria Rosa Ciriolo

Open access · goldAbstract readReview
In one paragraph

Review in Cancers, 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
2.2field-weighted citation impact, top 11% 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, 39 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

5 authors at 2 institutions in 1 country.

Serena CastelliDepartment of Biology, University of Rome "Tor Vergata", Via Della Ricerca Scientifica 1, 00133 Rome, Italy.
Pamela De FalcoDepartment of Biology, University of Rome "Tor Vergata", Via Della Ricerca Scientifica 1, 00133 Rome, Italy.
Fabio CiccaroneIRCCS San Raffaele Pisana, Department of Human Sciences and Promotion of the Quality of Life, San Raffaele Roma Open University, 00166 Rome, Italy.
Enrico DesideriDepartment of Biology, University of Rome "Tor Vergata", Via Della Ricerca Scientifica 1, 00133 Rome, Italy.ORCID 0000-0002-1884-7491
Maria Rosa CirioloDepartment of Biology, University of Rome "Tor Vergata", Via Della Ricerca Scientifica 1, 00133 Rome, Italy.
University of Rome Tor Vergata · ITIstituti di Ricovero e Cura a Carattere Scientifico · IT

Funding

Italian Association for Cancer Research IG 15403Ministry of Education, Universities and Research 2017A5TXC3
6 · The paper itself

Abstract

Although cancer cell metabolism was mainly considered to rely on glycolysis, with the concomitant impairment of mitochondrial metabolism, it has recently been demonstrated that several tumor types are sustained by oxidative phosphorylation (OXPHOS). In this context, endogenous fatty acids (FAs) deriving from lipolysis or lipophagy are oxidised into the mitochondrion, and are used as a source of energy through OXPHOS. Because the electron transport chain is the main source of ROS, cancer cells relying on fatty acid oxidation (FAO) need to be equipped with antioxidant systems that maintain the ROS levels under the death threshold. In those conditions, ROS can act as second messengers, favouring proliferation and survival. Herein, we highlight the different responses that tumor cells adopt when lipid catabolism is augmented, taking into account the different ROS fates. Many papers have demonstrated that the pro- or anti-tumoral roles of endogenous FA usage are hugely dependent on the tumor type, and on the capacity of cancer cells to maintain redox homeostasis. In light of this, clinical studies have taken advantage of the boosting of lipid catabolism to increase the efficacy of tumor therapy, whereas, in other contexts, antioxidant compounds are useful to reduce the pro-survival effects of ROS deriving from FAO.

Indexed as

fatty acid oxidationlipid catabolismmitochondrial metabolismreactive oxygen species

Identifiers

PMID34771647
PMCPMC8583096
OpenAlexW3210528556

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.