Evidence map›Paper›PMID 27385336›Full record

ArticleMolecular biology of the cell2016

AMPK activity regulates trafficking of mitochondria to the leading edge during cell migration and matrix invasion.

Brian Cunniff, Andrew J McKenzie, Nicholas H Heintz, Alan K Howe

Abstract read
In one paragraph

Article in Molecular biology of the cell, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 167 papers.

0numbers the graph read from it
0cells of the map it votes in
167citing papers in PubMed
–field-weighted citation impact
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

167 citing papers in PubMed.

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  15. Acquired motility ofProceedings of the National Academy of Sciences of the United States of America · 2026
    Article
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107 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

4 authors.

Brian CunniffDepartment of Pathology, University of Vermont, Burlington, VT 05405 University of Vermont Cancer Center, University of Vermont, Burlington, VT 05405.
Andrew J McKenzieUniversity of Vermont Cancer Center, University of Vermont, Burlington, VT 05405 Department of Pharmacology, University of Vermont, Burlington, VT 05405.
Nicholas H HeintzDepartment of Pathology, University of Vermont, Burlington, VT 05405 University of Vermont Cancer Center, University of Vermont, Burlington, VT 05405.
Alan K HoweUniversity of Vermont Cancer Center, University of Vermont, Burlington, VT 05405 Department of Pharmacology, University of Vermont, Burlington, VT 05405 alan.howe@med.uvm.edu.

Funding

Mechano-Chemical Regulation of GPCR/PKA Signaling During Cell MigrationR01GM117490 · NIGMS · UNIVERSITY OF VERMONT & ST AGRIC COLLEGE · PI HOWE, ALAN K · 2016 to 2019
$1.6M
Cross-talk between PKA, cellular tension, and Ca2+ channels during cell migrationR01GM097495 · NIGMS · UNIVERSITY OF VERMONT & ST AGRIC COLLEGE · PI HOWE, ALAN K · 2011 to 2014
$1.2M
NIGMS NIH HHS R01 GM097495NIGMS NIH HHS R01 GM117490
6 · The paper itself

Abstract

Cell migration is a complex behavior involving many energy-expensive biochemical events that iteratively alter cell shape and location. Mitochondria, the principal producers of cellular ATP, are dynamic organelles that fuse, divide, and relocate to respond to cellular metabolic demands. Using ovarian cancer cells as a model, we show that mitochondria actively infiltrate leading edge lamellipodia, thereby increasing local mitochondrial mass and relative ATP concentration and supporting a localized reversal of the Warburg shift toward aerobic glycolysis. This correlates with increased pseudopodial activity of the AMP-activated protein kinase (AMPK), a critically important cellular energy sensor and metabolic regulator. Furthermore, localized pharmacological activation of AMPK increases leading edge mitochondrial flux, ATP content, and cytoskeletal dynamics, whereas optogenetic inhibition of AMPK halts mitochondrial trafficking during both migration and the invasion of three-dimensional extracellular matrix. These observations indicate that AMPK couples local energy demands to subcellular targeting of mitochondria during cell migration and invasion.

Indexed as

Adenosine TriphosphateAMP-Activated Protein KinasesCell Line, TumorCell MovementCytoskeletonEnergy MetabolismFemaleGlycolysisHumansMitochondriaOvarian NeoplasmsPhosphorylationProtein TransportPseudopodiaAdenosine TriphosphateAMP-Activated Protein Kinases

Identifiers

PMID27385336
PMCPMC5007087

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.