Evidence map›Paper›PMID 30557378›Full record

ArticlePloS one2018

Tumor suppressor RARRES1- A novel regulator of fatty acid metabolism in epithelial cells.

Sara Maimouni, Naiem Issa, Selina Cheng, Chokri Ouaari, Amrita Cheema, Deepak Kumar, Stephen Byers

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
0.8field-weighted citation impact, top 32% 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

23 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
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  3. Genetic associations of LXN polymorphisms with toxicities of platinum-based concurrent chemoradiotherapy of nasopharyngeal carcinoma.Supportive care in cancer : official journal of the Multinational Association of Supportive Care in Cancer · 2026
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  11. Single-cell transcriptomic profiling of the mouse cochlea: An atlas for targeted therapies.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  12. Review
  13. 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 at 3 institutions in 1 country.

Sara MaimouniDepartment of Biochemical, Molecular and Cellular Biology, Georgetown University, Washington, District of Columbia, United States of America.ORCID 0000-0002-6085-0766
Naiem IssaGeorgetown-Lombardi Comprehensive Cancer Center, Department of Oncology, Georgetown University, Washington, District of Columbia, United States of America.
Selina ChengGeorgetown-Lombardi Comprehensive Cancer Center, Department of Oncology, Georgetown University, Washington, District of Columbia, United States of America.
Chokri OuaariGeorgetown-Lombardi Comprehensive Cancer Center, Department of Oncology, Georgetown University, Washington, District of Columbia, United States of America.
Amrita CheemaGeorgetown-Lombardi Comprehensive Cancer Center, Department of Oncology, Georgetown University, Washington, District of Columbia, United States of America.
Deepak KumarJulius L. Chambers Biomedical Biotechnology Research Institute, North Carolina Central University, Durham, North Carolina, United States of America.
Stephen ByersDepartment of Biochemical, Molecular and Cellular Biology, Georgetown University, Washington, District of Columbia, United States of America.ORCID 0000-0003-3036-3518
Georgetown University · USNorth Carolina Central University · USUniversity of the District of Columbia · US

Funding

Tissue Culture Shared ResourceP30CA051008 · NCI · GEORGETOWN UNIVERSITY · PI Habtom W Ressom · 1990 to 2026
$71.5M
NCI NIH HHS P30 CA051008
6 · The paper itself

Abstract

Retinoic acid receptor responder 1 (RARRES1) is silenced in many cancers and is differentially expressed in metabolism associated diseases, such as hepatic steatosis, hyperinsulinemia and obesity. Here we report a novel function of RARRES1 in metabolic reprogramming of epithelial cells. Using non-targeted LC-MS, we discovered that RARRES1 depletion in epithelial cells caused a global increase in lipid synthesis. RARRES1-depleted cells rewire glucose metabolism by switching from aerobic glycolysis to glucose-dependent de novo lipogenesis (DNL). Treatment with fatty acid synthase (FASN) inhibitor, C75, reversed the effects of RARRES1 depletion. The increased DNL in RARRES1-depleted normal breast and prostate epithelial cells proved advantageous to the cells during starvation, as the increase in fatty acid availability lead to more oxidized fatty acids (FAO), which were used for mitochondrial respiration. Expression of RARRES1 in several common solid tumors is also contextually correlated with expression of fatty acid metabolism genes and fatty acid-regulated transcription factors. Pathway enrichment analysis led us to determine that RARRES1 is regulated by peroxisome proliferating activated receptor (PPAR) signaling. These findings open up a new avenue for metabolic reprogramming and identify RARRES1 as a potential target for cancers and other diseases with impaired fatty acid metabolism.

Indexed as

Adenosine TriphosphateBreastBreast NeoplasmsCell LineColorectal NeoplasmsEpithelial CellsFatty AcidsFatty Acid SynthasesGene ExpressionGlucoseGlycolysisHumansLipid MetabolismLipogenesisMaleMembrane ProteinsAdenosine TriphosphateFatty AcidsFatty Acid SynthasesGlucoseMembrane ProteinsRARRES1 protein, human

Identifiers

PMID30557378
PMCPMC6296515
OpenAlexW2905477965

What Socratic 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 Socratic graph.