Evidence map›Paper›PMID 26351140›Full record

ArticleMolecular and cellular biology2015

AMPK Promotes Aberrant PGC1β Expression To Support Human Colon Tumor Cell Survival.

Kurt W Fisher, Binita Das, Hyun Seok Kim, Beth K Clymer, Drew Gehring, Deandra R Smith, Diane L Costanzo-Garvey, Mario R Fernandez, Michael G Brattain, David L Kelly and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in Molecular and cellular biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 1 pooled it
1.8field-weighted citation impact, top 15% 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, 1 synthesis or guideline pooled it, 39 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. The AMPK Pathway: Molecular Rejuvenation of Metabolism and Mitochondria.Annual review of cell and developmental biology · 2025
    Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. SOS1 and KSR1 modulate MEK inhibitor responsiveness to target resistant cell populations based on PI3K and KRAS mutation status.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Review
  17. LKB1/AMPK Pathway and Drug Response in Cancer: A Therapeutic Perspective.Oxidative medicine and cellular longevity · 2019
    Review
  18. Article
  19. Article
  20. AMPK: guardian of metabolism and mitochondrial homeostasis.Nature reviews. Molecular cell biology · 2018
    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

13 authors at 2 institutions in 1 country.

Kurt W FisherEppley Institute, University of Nebraska Medical Center, Omaha, Nebraska, USA.
Binita DasEppley Institute, University of Nebraska Medical Center, Omaha, Nebraska, USA.
Hyun Seok KimDepartment of Cell Biology, University of Texas Southwestern Medical Center, Dallas, Texas, USA.
Beth K ClymerEppley Institute, University of Nebraska Medical Center, Omaha, Nebraska, USA.
Drew GehringEppley Institute, University of Nebraska Medical Center, Omaha, Nebraska, USA.
Deandra R SmithEppley Institute, University of Nebraska Medical Center, Omaha, Nebraska, USA.
Diane L Costanzo-GarveyEppley Institute, University of Nebraska Medical Center, Omaha, Nebraska, USA.
Mario R FernandezEppley Institute, University of Nebraska Medical Center, Omaha, Nebraska, USA.
Michael G BrattainEppley Institute, University of Nebraska Medical Center, Omaha, Nebraska, USA Fred & Pamela Buffett Cancer Center, University of Nebraska Medical Center, Omaha, Nebraska, USA.
David L KellyEppley Institute, University of Nebraska Medical Center, Omaha, Nebraska, USA.
John MacMillanDepartment of Biochemistry, University of Texas Southwestern Medical Center, Dallas Texas, USA.
Michael A WhiteDepartment of Cell Biology, University of Texas Southwestern Medical Center, Dallas, Texas, USA Michael.White@utsouthwestern.edu rlewis@unmc.edu.
Robert E LewisEppley Institute, University of Nebraska Medical Center, Omaha, Nebraska, USA Michael.White@utsouthwestern.edu rlewis@unmc.edu.
University of Nebraska Medical Center · USThe University of Texas Southwestern 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
CHEMICAL CARCINOGENESIS &CANCER BIOLOGYT32CA009476 · NCI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI Jennifer D. Black · 1988 to 2026
$6.2M
COMPONENTS OF RAS-MEDIATED GROWTH CONTROLR01CA071443 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI WHITE, MICHAEL A. · 1996 to 2015
$4.8M
Cell Survival Determinants of Metastasis in IGF1R-Dependent CRCR01CA054807 · NCI · UNIVERSITY OF TOLEDO HEALTH SCI CAMPUS · PI BLACK, JENNIFER D. · 1991 to 2016
$3.7M
Marine Actinomycetes as a Resource for Anticancer Natural ProductsR01CA149833 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI MACMILLAN, JOHN B · 2010 to 2014
$1.6M
Novel Effectors of Colon TumorigenesisR01CA157774 · NCI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI LEWIS, ROBERT E. · 2012 to 2016
$1.5M
Targeting Mechanistic Subtypes of Neoplastic DiseaseR35CA197717 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI WHITE, MICHAEL A. · 2015 to 2015
$725k
Discovering Vulnerabilities in Ras-driven CancersF30CA203397 · NCI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI NEILSEN, BETH · 2016 to 2019
$165k
NCI NIH HHS CA071443NCI NIH HHS CA1499833NCI NIH HHS CA157774NCI NIH HHS F30 CA203397NCI NIH HHS P30 CA036727NCI NIH HHS P30CA036727NCI NIH HHS R01 CA054807NCI NIH HHS R01 CA071443NCI NIH HHS R01 CA149833NCI NIH HHS R01 CA157774NCI NIH HHS R35 CA197717NCI NIH HHS T32 CA009476NCI NIH HHS T32CA009476
6 · The paper itself

Abstract

A major goal of cancer research is the identification of tumor-specific vulnerabilities that can be exploited for the development of therapies that are selectively toxic to the tumor. We show here that the transcriptional coactivators peroxisome proliferator-activated receptor gamma coactivator 1β (PGC1β) and estrogen-related receptor α (ERRα) are aberrantly expressed in human colon cell lines and tumors. With kinase suppressor of Ras 1 (KSR1) depletion as a reference standard, we used functional signature ontology (FUSION) analysis to identify the γ1 subunit of AMP-activated protein kinase (AMPK) as an essential contributor to PGC1β expression and colon tumor cell survival. Subsequent analysis revealed that a subunit composition of AMPK (α2β2γ1) is preferred for colorectal cancer cell survival, at least in part, by stabilizing the tumor-specific expression of PGC1β. In contrast, PGC1β and ERRα are not detectable in nontransformed human colon epithelial cells, and depletion of the AMPKγ1 subunit has no effect on their viability. These data indicate that Ras oncogenesis relies on the aberrant activation of a PGC1β-dependent transcriptional pathway via a specific AMPK isoform.

Indexed as

Gene Expression Regulation, NeoplasticAMP-Activated Protein KinasesAnimalsCarrier ProteinsCell Line, TumorCell SurvivalColonColonic NeoplasmsERRalpha Estrogen-Related ReceptorHumansMice, Inbred BALB CMice, NudeProtein KinasesProtein SubunitsReceptors, EstrogenRNA-Binding ProteinsAMP-Activated Protein KinasesCarrier ProteinsERRalpha Estrogen-Related ReceptorKSR-1 protein kinasePPARGC1B protein, humanPRKAA2 protein, humanPRKAB2 protein, humanPRKAG1 protein, humanProtein KinasesProtein SubunitsReceptors, EstrogenRNA-Binding Proteins

Identifiers

PMID26351140
PMCPMC4609747
OpenAlexW2135996922

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.