Evidence map›Paper›PMID 33811729›Full record

ArticleThe FEBS journal2021

Differential substrate use in EGF- and oncogenic KRAS-stimulated human mammary epithelial cells.

Mark A Keibler, Wentao Dong, Keegan D Korthauer, Aaron M Hosios, Sun Jin Moon, Lucas B Sullivan, Nian Liu, Keene L Abbott, Orlando D Arevalo, Kailing Ho and 7 more

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The FEBS journal, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.4field-weighted citation impact, top 47% 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

2 citing papers in PubMed, 6 citations in OpenAlex.

  1. Review
  2. Isotope tracing in health and disease.Current opinion in biotechnology · 2022
    Review
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

17 authors at 5 institutions in 1 country.

Mark A KeiblerDepartment of Chemical Engineering, Massachusetts Institute of Technology, Cambridge, MA, USA.ORCID 0000-0002-5410-6543
Wentao DongDepartment of Chemical Engineering, Massachusetts Institute of Technology, Cambridge, MA, USA.
Keegan D KorthauerDepartment of Biostatistics & Computational Biology, Dana-Farber Cancer Institute, Boston, MA, USA.
Aaron M HosiosDepartment of Biology, Massachusetts Institute of Technology, Cambridge, MA, USA.
Sun Jin MoonDepartment of Chemical Engineering, Massachusetts Institute of Technology, Cambridge, MA, USA.
Lucas B SullivanDepartment of Biology, Massachusetts Institute of Technology, Cambridge, MA, USA.ORCID 0000-0002-6745-8222
Nian LiuDepartment of Chemical Engineering, Massachusetts Institute of Technology, Cambridge, MA, USA.
Keene L AbbottDepartment of Biology, Massachusetts Institute of Technology, Cambridge, MA, USA.
Orlando D ArevaloDepartment of Chemical Engineering, Massachusetts Institute of Technology, Cambridge, MA, USA.
Kailing HoDepartment of Chemistry, Wellesley College, Wellesley, MA, USA.
Jennifer LeeDepartment of Biology, Massachusetts Institute of Technology, Cambridge, MA, USA.
Aasavari S PhanseDepartment of Electrical Engineering & Computer Science, Massachusetts Institute of Technology, Cambridge, MA, USA.
Joanne K KelleherDepartment of Chemical Engineering, Massachusetts Institute of Technology, Cambridge, MA, USA.
Othon IliopoulosCenter for Cancer Research, Massachusetts General Hospital Cancer Center, Charlestown, MA, USA.
Jonathan L ColoffDepartment of Cell Biology, Harvard Medical School, Boston, MA, USA.
Matthew G Vander HeidenDepartment of Biology, Massachusetts Institute of Technology, Cambridge, MA, USA.ORCID 0000-0002-6702-4192
Gregory StephanopoulosDepartment of Chemical Engineering, Massachusetts Institute of Technology, Cambridge, MA, USA.
Massachusetts Institute of Technology · USHarvard University · USDana-Farber Cancer Institute · USMassachusetts General Hospital · USWellesley College · US

Funding

VIRUS PRODUCTION COREP30CA014051 · NCI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI MATTHEW G. VANDER HEIDEN · 1985 to 2026
$93.9M
PRE-DOCTORAL TRAINING IN THE BIOLOGICAL SCIENCEST32GM007287 · NIGMS · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI BELL, STEPHEN P., KEATING, AMY E · 1985 to 2019
$40.8M
Understanding the role of metabolism in cancerR35CA242379 · NCI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI VANDER HEIDEN, MATTHEW G. · 2019 to 2025
$5.8M
Chemical Biology of IRP1-HIF2a SignalingR01CA215431 · NCI · MASSACHUSETTS GENERAL HOSPITAL · PI ILIOPOULOS, OTHON · 2017 to 2021
$3.1M
Analysis of cancer cell metabolism in diverse environmental conditionsR01CA201276 · NCI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI VANDER HEIDEN, MATTHEW G., VITKUP, DENNIS · 2016 to 2020
$3.0M
Regulation of glucose metabolism to allow tumor initiation and growthR01CA168653 · NCI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI VANDER HEIDEN, MATTHEW G. · 2013 to 2019
$1.9M
Hypoxia-induced Metabolic Changes in CancerR01CA160458 · NCI · MASSACHUSETTS GENERAL HOSPITAL · PI ILIOPOULOS, OTHON, STEPHANOPOULOS, GREGORY · 2012 to 2016
$1.6M
Elucidating modulators of hepatic metabolism by quantitative flux analysisR01DK075850 · NIDDK · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI STEPHANOPOULOS, GREGORY · 2006 to 2010
$1.5M
Howard Hughes Medical InstituteNCI NIH HHS P30 CA014051NCI NIH HHS R01 CA160458NCI NIH HHS R01 CA168653NCI NIH HHS R01 CA201276NCI NIH HHS R01 CA215431NCI NIH HHS R35 CA242379NIDDK NIH HHS R01 DK075850NIGMS NIH HHS T32 GM007287
6 · The paper itself

Abstract

Many metabolic phenotypes in cancer cells are also characteristic of proliferating nontransformed mammalian cells, and attempts to distinguish between phenotypes resulting from oncogenic perturbation from those associated with increased proliferation are limited. Here, we examined the extent to which metabolic changes corresponding to oncogenic KRAS expression differed from those corresponding to epidermal growth factor (EGF)-driven proliferation in human mammary epithelial cells (HMECs). Removal of EGF from culture medium reduced growth rates and glucose/glutamine consumption in control HMECs despite limited changes in respiration and fatty acid synthesis, while the relative contribution of branched-chain amino acids to the TCA cycle and lipogenesis increased in the near-quiescent conditions. Most metabolic phenotypes measured in HMECs expressing mutant KRAS were similar to those observed in EGF-stimulated control HMECs that were growing at comparable rates. However, glucose and glutamine consumption as well as lactate and glutamate production were lower in KRAS-expressing cells cultured in media without added EGF, and these changes correlated with reduced sensitivity to GLUT1 inhibitor and phenformin treatment. Our results demonstrate the strong dependence of metabolic behavior on growth rate and provide a model to distinguish the metabolic influences of oncogenic mutations and nononcogenic growth.

Indexed as

AnimalsBreastBreast NeoplasmsCarcinogenesisCell ProliferationEpidermal Growth FactorEpithelial CellsFemaleGene Expression Regulation, NeoplasticGlucoseGlucose Transporter Type 1Glutamic AcidGlutamineHumansLactic AcidMammary Glands, HumanEpidermal Growth FactorGlucoseGlucose Transporter Type 1Glutamic AcidGlutamineKRAS protein, humanLactic AcidProto-Oncogene Proteins p21(ras)SLC2A1 protein, humanbranched-chain amino acidscancer metabolismcell growthcell proliferationKRAS

Identifiers

PMID33811729
PMCPMC8487438
OpenAlexW3148232362

What OpenQuestion holds

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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.