Evidence map›Paper›PMID 24073224›Full record

ArticlePloS one2013

Secreted human adipose leptin decreases mitochondrial respiration in HCT116 colon cancer cells.

Einav Yehuda-Shnaidman, Lili Nimri, Tanya Tarnovscki, Boris Kirshtein, Assaf Rudich, Betty Schwartz

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing 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

17 citing papers in PubMed, 25 citations in OpenAlex.

  1. Review
  2. Review
  3. Obesity: a perfect storm for carcinogenesis.Cancer metastasis reviews · 2022
    Review
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  6. Review
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  8. Article
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  14. The anti-oncogenic influence of ellagic acid on colon cancer cells in leptin-enriched microenvironment.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Article
  15. Article
  16. Adipose tissue dysfunction and its effects on tumor metabolism.Hormone molecular biology and clinical investigation · 2015
    Review
  17. 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

6 authors at 3 institutions in 1 country.

Einav Yehuda-ShnaidmanInstitute of Biochemistry, Food Science and Nutrition, The Robert H. Smith Faculty of Agriculture, Food and Environment, the Hebrew University of Jerusalem, Rehovot, Israel.
Lili Nimri
Tanya Tarnovscki
Boris Kirshtein
Assaf Rudich
Betty Schwartz
Hebrew University of Jerusalem · ILBen-Gurion University of the Negev · ILSoroka Medical Center · IL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Obesity is a key risk factor for the development of colon cancer; however, the endocrine/paracrine/metabolic networks mediating this connection are poorly understood. Here we hypothesize that obesity results in secreted products from adipose tissue that induce malignancy-related metabolic alterations in colon cancer cells. Human HCT116 colon cancer cells, were exposed to conditioned media from cultured human adipose tissue fragments of obese vs. non-obese subjects. Oxygen consumption rate (OCR, mostly mitochondrial respiration) and extracellular acidification rate (ECAR, mostly lactate production via glycolysis) were examined vis-à-vis cell viability and expression of related genes and proteins. Our results show that conditioned media from obese (vs. non-obese) subjects decreased basal (40%, p<0.05) and maximal (50%, p<0.05) OCR and gene expression of mitochondrial proteins and Bax without affecting cell viability or expression of glycolytic enzymes. Similar changes could be recapitulated by incubating cells with leptin, whereas, leptin-receptor specific antagonist inhibited the reduced OCR induced by conditioned media from obese subjects. We conclude that secreted products from the adipose tissue of obese subjects inhibit mitochondrial respiration and function in HCT116 colon cancer cells, an effect that is at least partly mediated by leptin. These results highlight a putative novel mechanism for obesity-associated risk of gastrointestinal malignancies, and suggest potential new therapeutic avenues.

Indexed as

Adipose TissueAdultBlotting, WesternCell RespirationCell SurvivalColonic NeoplasmsCulture Media, ConditionedGlycolysisHumansLeptinMiddle AgedMitochondriaMitochondrial ProteinsObesityOxygen ConsumptionReal-Time Polymerase Chain ReactionCulture Media, ConditionedLeptinMitochondrial ProteinsRNA, Messenger

Identifiers

PMID24073224
PMCPMC3779244
OpenAlexW2018670732

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.