Evidence map›Paper›PMID 28151470›Full record

ArticleCell death & disease2017

Adipocytes activate mitochondrial fatty acid oxidation and autophagy to promote tumor growth in colon cancer.

Yang-An Wen, Xiaopeng Xing, Jennifer W Harris, Yekaterina Y Zaytseva, Mihail I Mitov, Dana L Napier, Heidi L Weiss, B Mark Evers, Tianyan Gao

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 192 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
192citing papers in PubMed, 1 pooled it
10.1field-weighted citation impact, top 1% 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

192 citing papers in PubMed, 1 synthesis or guideline pooled it, 280 citations in OpenAlex.

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  13. Frontiers in pharmacology · 2026
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132 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

9 authors at 1 institution in 1 country.

Yang-An WenMarkey Cancer Center, University of Kentucky, Lexington, KY, USA.
Xiaopeng XingMarkey Cancer Center, University of Kentucky, Lexington, KY, USA.
Jennifer W HarrisMarkey Cancer Center, University of Kentucky, Lexington, KY, USA.
Yekaterina Y ZaytsevaMarkey Cancer Center, University of Kentucky, Lexington, KY, USA.
Mihail I MitovMarkey Cancer Center, University of Kentucky, Lexington, KY, USA.ORCID 0000-0001-9101-5053
Dana L NapierMarkey Cancer Center, University of Kentucky, Lexington, KY, USA.
Heidi L WeissMarkey Cancer Center, University of Kentucky, Lexington, KY, USA.
B Mark EversMarkey Cancer Center, University of Kentucky, Lexington, KY, USA.
Tianyan GaoMarkey Cancer Center, University of Kentucky, Lexington, KY, USA.
University of Kentucky · US

Funding

University of Kentucky Markey Cancer Center Support Grant ECIA SupplementP30CA177558 · NCI · UNIVERSITY OF KENTUCKY · PI KATHLEEN L. O'CONNOR · 2013 to 2026
$38.3M
Kentucky Center for Clinical and Translational ScienceUL1TR000117 · NCATS · UNIVERSITY OF KENTUCKY · PI KERN, PHILIP A · 2012 to 2015
$13.3M
The Role of PHLPP in Colon CancerR01CA133429 · NCI · UNIVERSITY OF TEXAS MED BR GALVESTON · PI GAO, TIANYAN · 2009 to 2024
$5.6M
Altered Lipid Metabolism as a Novel Target for Colon Cancer TreatmentR01CA208343 · NCI · UNIVERSITY OF KENTUCKY · PI EVERS, BERNARD MARK, GAO, TIANYAN · 2017 to 2021
$2.1M
NCATS NIH HHS UL1 TR000117NCI NIH HHS P30 CA177558NCI NIH HHS R01 CA133429NCI NIH HHS R01 CA208343
6 · The paper itself

Abstract

Obesity has been associated with increased incidence and mortality of a wide variety of human cancers including colorectal cancer. However, the molecular mechanism by which adipocytes regulate the metabolism of colon cancer cells remains elusive. In this study, we showed that adipocytes isolated from adipose tissues of colon cancer patients have an important role in modulating cellular metabolism to support tumor growth and survival. Abundant adipocytes were found in close association with invasive tumor cells in colon cancer patients. Co-culture of adipocytes with colon cancer cells led to a transfer of free fatty acids that released from the adipocytes to the cancer cells. Uptake of fatty acids allowed the cancer cells to survive nutrient deprivation conditions by upregulating mitochondrial fatty acid β-oxidation. Mechanistically, co-culture of adipocytes or treating cells with fatty acids induced autophagy in colon cancer cells as a result of AMPK activation. Inhibition of autophagy attenuated the ability of cancer cells to utilize fatty acids and blocked the growth-promoting effect of adipocytes. In addition, we found that adipocytes stimulated the expression of genes associated with cancer stem cells and downregulated genes associated with intestinal epithelial cell differentiation in primary colon cancer cells and mouse tumor organoids. Importantly, the presence of adipocytes promoted the growth of xenograft tumors in vivo. Taken together, our results show that adipocytes in the tumor microenvironment serve as an energy provider and a metabolic regulator to promote the growth and survival of colon cancer cells.

Indexed as

AdipocytesAdipose TissueAMP-Activated Protein KinasesAnimalsAutophagyCell DifferentiationCell LineCell Line, TumorCoculture TechniquesColonic NeoplasmsDown-RegulationEpithelial CellsFatty AcidsGene ExpressionHumansLipid MetabolismAMP-Activated Protein KinasesFatty Acids

Identifiers

PMID28151470
PMCPMC5386470
OpenAlexW2583960272

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.