Evidence map›Paper›PMID 28464016›Full record

ArticlePloS one2017

MUC1 facilitates metabolomic reprogramming in triple-negative breast cancer.

Gennifer Goode, Venugopal Gunda, Nina V Chaika, Vinee Purohit, Fang Yu, Pankaj K Singh

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
1.8field-weighted citation impact, top 16% 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, 42 citations in OpenAlex.

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  6. The MUC1-HIF-1α signaling axis regulates pancreatic cancer pathogenesis through polyamine metabolism remodeling.Proceedings of the National Academy of Sciences of the United States of America · 2024
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  14. Impact of the PdInternational journal of molecular sciences · 2021
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

Gennifer GoodeThe Eppley Institute for Research in Cancer and Allied Diseases, University of Nebraska Medical Center, Omaha, Nebraska, United States of America.
Venugopal GundaThe Eppley Institute for Research in Cancer and Allied Diseases, University of Nebraska Medical Center, Omaha, Nebraska, United States of America.
Nina V ChaikaThe Eppley Institute for Research in Cancer and Allied Diseases, University of Nebraska Medical Center, Omaha, Nebraska, United States of America.
Vinee PurohitThe Eppley Institute for Research in Cancer and Allied Diseases, University of Nebraska Medical Center, Omaha, Nebraska, United States of America.
Fang YuDepartment of Biostatistics, University of Nebraska Medical Center, Omaha, Nebraska, United States of America.
Pankaj K SinghThe Eppley Institute for Research in Cancer and Allied Diseases, University of Nebraska Medical Center, Omaha, Nebraska, United States of America.ORCID http://orcid.org/0000-0001-8903-0131
University of Nebraska Medical Center · US

Funding

UNMC/EPPLEY CANCER CENTER SUPPORT GRANTP30CA036727 · NCI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI Apar Kishor Ganti · 1985 to 2026
$55.0M
Tissue CoreP50CA127297 · NCI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI HOLLINGSWORTH, MICHAEL A. · 2008 to 2018
$17.1M
Targeting Tumor-Stromal Metabolic Cross-Talk in Pancreatic CancerR01CA163649 · NCI · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI Pankaj Kumar Singh · 2012 to 2026
$5.4M
Research Pilot Project ProgramP30GM106397 · NIGMS · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI JOHNSON, KEITH R · 2013 to 2017
$4.9M
Metabolic Regulation of Tumor Progression, Metastasis and Chemoresistance by SIRT5/ELK3 signaling in Pancreatic CancerR01CA216853 · NCI · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI SINGH, PANKAJ KUMAR · 2017 to 2021
$2.6M
Targeting the Metabolic Basis of Cachexia in Pancreatic CancerR01CA210439 · NCI · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI SINGH, PANKAJ KUMAR · 2017 to 2021
$2.6M
NCI NIH HHS P50 CA127297NCI NIH HHS R01 CA163649NCI NIH HHS R01 CA210439NCI NIH HHS R01 CA216853NIGMS NIH HHS P30 GM106397
6 · The paper itself

Abstract

backgroundMucin1 (MUC1), a glycoprotein associated with chemoresistance and an aggressive cancer phenotype, is aberrantly overexpressed in triple-negative breast cancer (TNBC). Recent studies suggest that MUC1 plays a role in modulating cancer cell metabolism and thereby supports tumor growth. Herein, we examined the role of MUC1 in metabolic reprogramming in TNBC.

methodsMUC1 was stably overexpressed in MDA-MB-231 TNBC cells and stably knocked down in MDA-MB-468 cells. We performed liquid chromatography-coupled tandem mass spectrometry-assisted metabolomic analyses and physiological assays, which indicated significant alterations in the metabolism of TNBC cells due to MUC1 expression.

resultsDifferential analyses identified significant differences in metabolic pathways implicated in cancer cell growth. In particular, MUC1 expression altered glutamine dependency of the cells, which can be attributed in part to the changes in the expression of genes that regulate glutamine metabolism, as observed by real-time PCR analysis. Furthermore, MUC1 expression altered the sensitivity of cells to transaminase inhibitor aminooxyacetate (AOA), potentially by altering glutamine metabolism.

conclusionsCollectively, these results suggest that MUC1 serves as a metabolic regulator in TNBC, facilitating the metabolic reprogramming of glutamine utilization that influences TNBC tumor growth.

Indexed as

MetabolomeCell Line, TumorCell ProliferationCell SurvivalCellular ReprogrammingChromatography, LiquidGene Expression Regulation, NeoplasticGene Knockdown TechniquesGlucoseGlutamineHumansMucin-1NitrogenReal-Time Polymerase Chain ReactionTandem Mass SpectrometryTriple Negative Breast NeoplasmsGlucoseGlutamineMUC1 protein, humanMucin-1Nitrogen

Identifiers

PMID28464016
PMCPMC5413086
OpenAlexW2610990377

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.