Evidence map›Paper›PMID 24418822›Full record

ArticleCell cycle (Georgetown, Tex.)2014

De novo fatty acid synthesis at the mitotic exit is required to complete cellular division.

Natalia Scaglia, Svitlana Tyekucheva, Giorgia Zadra, Cornelia Photopoulos, Massimo Loda

Open access · bronzeAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed
3.7field-weighted citation impact, top 8% 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

61 citing papers in PubMed, 104 citations in OpenAlex.

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  19. Metabolic Alterations in Canine Mammary Tumors.Animals : an open access journal from MDPI · 2023
    Review
  20. Article

1 more citing papers are in PubMed but not listed here.

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.

Natalia ScagliaDepartment of Medical Oncology; Dana-Farber Cancer Institute; Harvard Medical School; Boston, MA USA.
Svitlana TyekuchevaDepartment of Biostatistics and Computational Biology; Dana-Farber Cancer Institute; Boston, MA USA; Department of Biostatistics; Harvard School of Public Health; Boston, MA USA.
Giorgia ZadraDepartment of Medical Oncology; Dana-Farber Cancer Institute; Harvard Medical School; Boston, MA USA; Department of Pathology; Brigham and Women's Hospital; Harvard Medical School; Boston, MA USA.
Cornelia PhotopoulosDepartment of Medical Oncology; Dana-Farber Cancer Institute; Harvard Medical School; Boston, MA USA.
Massimo LodaDepartment of Medical Oncology; Dana-Farber Cancer Institute; Harvard Medical School; Boston, MA USA; Center for Molecular Oncologic Pathology; Dana-Farber Cancer Institute; Harvard Medical School; Boston, MA USA; Department of Pathology; Brigham and Women's Hospital; Harvard Medical School; Boston, MA USA; The Broad Institute; Cambridge, MA USA; Division of Cancer Studies; King's College London; London, UK.
Dana-Farber Cancer Institute · USBrigham and Women's Hospital · US

Funding

Tumor and Circulating Markers as Links Between Obesity and Lethal Prostate CanceP50CA090381 · NCI · DANA-FARBER CANCER INSTITUTE · PI LODA, MASSIMO · 2002 to 2017
$36.2M
Molecular Link Between Metabolic Syndrome and Prostate CancerR01CA131945 · NCI · DANA-FARBER CANCER INST · PI LODA, MASSIMO · 2008 to 2018
$4.0M
NCI NIH HHS P50 CA090381NCI NIH HHS P50 CA90381NCI NIH HHS R01 CA131945NCI NIH HHS R01CA131945
6 · The paper itself

Abstract

Although the regulation of the cell cycle has been extensively studied, much less is known about its coordination with the cellular metabolism. Using mass spectrometry we found that lysophospholipid levels decreased drastically from G 2/M to G 1 phase, while de novo phosphatidylcholine synthesis, the main phospholipid in mammalian cells, increased, suggesting that enhanced membrane production was concomitant to a decrease in its turnover. In addition, fatty acid synthesis and incorporation into membranes was increased upon cell division. The rate-limiting reaction for de novo fatty acid synthesis is catalyzed by acetyl-CoA carboxylase. As expected, its inhibiting phosphorylation decreased prior to cytokinesis initiation. Importantly, the inhibition of fatty acid synthesis arrested the cells at G 2/M despite the presence of abundant fatty acids in the media. Our results suggest that de novo lipogenesis is essential for cell cycle completion. This "lipogenic checkpoint" at G 2/M may be therapeutically exploited for hyperproliferative diseases such as cancer.

Indexed as

Acetyl-CoA CarboxylaseAMP-Activated Protein KinasesCell DivisionFatty AcidsG1 PhaseG2 Phase Cell Cycle CheckpointsHeLa CellsHumansMetabolic Networks and PathwaysMitosisAcetyl-CoA CarboxylaseAMP-Activated Protein KinasesFatty AcidsAMPKC75cell cyclecell cycle arrestde novo lipogenesisfatty acidlysophospholipidmetabolomephospholipid

Identifiers

PMID24418822
PMCPMC3979921
OpenAlexW1982116171

What OpenQuestion holds

Textmetadata
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.