Evidence map›Paper›PMID 33710603›Full record

ArticleCellular oncology (Dordrecht, Netherlands)2021

Survivin drives tumor-associated macrophage reprogramming: a novel mechanism with potential impact for obesity.

E Benaiges, V Ceperuelo-Mallafré, A Madeira, R Bosch, C Núñez-Roa, M Ejarque, E Maymó-Masip, I Huber-Ruano, M Lejeune, J Vendrell and 1 more

Open access · hybridAbstract read
In one paragraph

Article in Cellular oncology (Dordrecht, Netherlands), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

11 citing papers in PubMed, 22 citations in OpenAlex.

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  8. Anti-TNF Therapies Suppress Adipose Tissue Inflammation in Crohn's Disease.International journal of molecular sciences · 2022
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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

11 authors at 3 institutions in 1 country.

E Benaiges *Institut d'Investigació Sanitària Pere Virgili, Endocrinology and Nutrition Service, Hospital Universitari de Tarragona Joan XXIII, 43007, Tarragona, Spain.
V Ceperuelo-Mallafré *Institut d'Investigació Sanitària Pere Virgili, Endocrinology and Nutrition Service, Hospital Universitari de Tarragona Joan XXIII, 43007, Tarragona, Spain.
A MadeiraInstitut d'Investigació Sanitària Pere Virgili, Endocrinology and Nutrition Service, Hospital Universitari de Tarragona Joan XXIII, 43007, Tarragona, Spain.
R BoschGrup de Recerca en Patologia Oncològica i Bioinformàtica, Molecular Biology and Research Section, Hospital de Tortosa Verge de la Cinta, IISPV, URV, 43500, Tortosa, Spain.
C Núñez-RoaInstitut d'Investigació Sanitària Pere Virgili, Endocrinology and Nutrition Service, Hospital Universitari de Tarragona Joan XXIII, 43007, Tarragona, Spain.
M EjarqueInstitut d'Investigació Sanitària Pere Virgili, Endocrinology and Nutrition Service, Hospital Universitari de Tarragona Joan XXIII, 43007, Tarragona, Spain.
E Maymó-MasipInstitut d'Investigació Sanitària Pere Virgili, Endocrinology and Nutrition Service, Hospital Universitari de Tarragona Joan XXIII, 43007, Tarragona, Spain.
I Huber-RuanoInstitut d'Investigació Sanitària Pere Virgili, Endocrinology and Nutrition Service, Hospital Universitari de Tarragona Joan XXIII, 43007, Tarragona, Spain.
M LejeuneGrup de Recerca en Patologia Oncològica i Bioinformàtica, Molecular Biology and Research Section, Hospital de Tortosa Verge de la Cinta, IISPV, URV, 43500, Tortosa, Spain.
J Vendrell *Institut d'Investigació Sanitària Pere Virgili, Endocrinology and Nutrition Service, Hospital Universitari de Tarragona Joan XXIII, 43007, Tarragona, Spain. jvo@comt.es.
S Fernández-Veledo *Institut d'Investigació Sanitària Pere Virgili, Endocrinology and Nutrition Service, Hospital Universitari de Tarragona Joan XXIII, 43007, Tarragona, Spain. sonia.fernandezveledo@gmail.com.ORCID http://orcid.org/0000-0003-2906-3788
Instituto de Salud Carlos III · ESHospital Universitari de Tortosa Verge de la Cinta · ESInstitut de Recerca Biomèdica Catalunya Sud · ES

Funding

Instituto de Salud Carlos III PI14/00228Instituto de Salud Carlos III PI17/0153Ministerio de Ciencia, Innovación y Universidades RTI2018-093919Ministerio de Ciencia, Innovación y Universidades SAF2015-65019-R
6 · The paper itself

Abstract

purposeRecent studies point to adipose-derived stem cells (ASCs) as a link between obesity and cancer. We aimed to determine whether survivin, which is highly secreted by ASCs from subjects with obesity, might drive a pro-tumoral phenotype in macrophages.

methodsThe effect of ASC conditioned medium on the macrophage phenotype was assessed by expression studies. Survivin intracellular localization and internalization were examined by subcellular fractionation and immunofluorescence, respectively. Loss- and gain-of-function studies were performed using adenoviral vectors, and gene expression patterns, migration and invasion capacities of cancer cells were examined. Heterotypic cultures of ASCs, macrophages and cancer cells were established to mimic the tumor microenvironment. Survivin-blocking experiments were used to determine the impact of survivin on both macrophages and cancer cells. Immunohistochemical analysis of survivin was performed in macrophages from ascitic fluids of cancer patients and healthy controls.

resultsWe found that obese-derived ASCs induced a phenotypic switch in macrophages characterized by the expression of both pro- and anti-inflammatory markers. Macrophages were found to internalize extracellular survivin, generating hybrid macrophages with a tumor-associated phenotype that included secretion of survivin. Exogenous expression of survivin in macrophages generated a similar phenotype and enhanced the malignant characteristics of cancer cells by a mechanism dependent on survivin phosphorylation at threonine 34. Survivin secreted by both ASCs from subjects with obesity and tumor-associated macrophages synergistically boosted the malignancy of cancer cells. Importantly, survivin was mainly detected in ascites-associated macrophages from patients with a malignant diagnosis.

conclusionOur data indicate that survivin may serve as a molecular link between obesity and cancer and as a novel marker for tumor-associated macrophages.

Indexed as

Adipose TissueCaco-2 CellsCells, CulturedGene Expression ProfilingGene Expression Regulation, NeoplasticHEK293 CellsHep G2 CellsHT29 CellsHumansNeoplasmsObesityPhenotypeStem CellsSurvivinTHP-1 CellsTumor-Associated MacrophagesBIRC5 protein, humanSurvivinAdipose-derived stem cellsCancerObesitySurvivinTumor-associated macrophages

Identifiers

PMID33710603
PMCPMC8338861
OpenAlexW3135474292

What OpenQuestion holds

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Registered trials

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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.