Evidence map›Paper›PMID 26848978›Full record

ArticleOncotarget2016

Loss of oncogenic miR-155 in tumor cells promotes tumor growth by enhancing C/EBP-β-mediated MDSC infiltration.

Sinae Kim, Jin Hoi Song, Seokho Kim, Peng Qu, Betty K Martin, Waheed S Sehareen, Diana C Haines, Pengnian C Lin, Shyam K Sharan, Suhwan Chang

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.1field-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

23 citing papers in PubMed, 35 citations in OpenAlex.

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  10. Breast Cancer and Anaesthesia: Genetic Influence.International journal of molecular sciences · 2021
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  17. lncRNAs in Non-Malignant Tissue Have Prognostic Value in Colorectal Cancer.International journal of molecular sciences · 2018
    Article
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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

10 authors at 5 institutions in 2 countries.

Sinae KimDepartment of Biomedical Sciences, Department of Physiology, University of Ulsan School of Medicine, Seoul, South Korea.
Jin Hoi SongAging Research Center, Korea Research Institute of Bioscience & Biotechnology, Taejeon, South Korea.
Seokho KimAging Research Center, Korea Research Institute of Bioscience & Biotechnology, Taejeon, South Korea.
Peng QuMouse Cancer Genetics Program, National Cancer Institute, Frederick, MD, USA.
Betty K MartinMouse Cancer Genetics Program, National Cancer Institute, Frederick, MD, USA.
Waheed S SehareenMouse Cancer Genetics Program, National Cancer Institute, Frederick, MD, USA.
Diana C HainesPathology Histotechnology Laboratory, Leidos Inc., Frederick National Laboratory for Cancer, Frederick, MD, USA.
Pengnian C LinMouse Cancer Genetics Program, National Cancer Institute, Frederick, MD, USA.
Shyam K SharanMouse Cancer Genetics Program, National Cancer Institute, Frederick, MD, USA.
Suhwan ChangDepartment of Biomedical Sciences, Department of Physiology, University of Ulsan School of Medicine, Seoul, South Korea.
Korea Research Institute of Bioscience and Biotechnology · KRNational Cancer Institute · USCancer Genetics (United States) · USLeidos (United States) · USUniversity of Ulsan · KR

Funding

Vascular Biology SectionZIABC011390 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI LIN, PENGNIAN · 2011 to 2020
$15.4M
Functional Evaluation of BRCA2 Variants on TumorigenesisZIABC010387 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI SHARAN, SHYAM · 2009 to 2025
$12.5M
6 · The paper itself

Abstract

The oncogenic role of microRNA-155 (miR-155) in leukemia is well established but its role in other cancers, especially breast cancer, is gradually emerging. In this study we examined the effect of mir-155 loss in a well-characterized spontaneous breast cancer mouse model where Brca1 and Trp53 are deleted by K14-Cre. miR-155 is known to be up-regulated in BRCA1-deficient tumors. Surprisingly, complete loss of miR-155 (miR-155ko/ko) did not alter the tumor free survival of the mutant mice. However, we found increased infiltration of myeloid derived suppressor cells (MDSCs) in miR-155 deficient tumors. In addition, cytokine/chemokine array analysis revealed altered level of cytokines that are implicated in the recruitment of MDSCs. Mechanistically, we identified C/EBP-β, a known miR-155 target, to regulate the expression of these cytokines in the miR-155-deficient cells. Furthermore, using an allograft model, we showed that inhibition of miR-155 in cancer cells suppressed in vivo growth, which was restored by the loss of miR-155 in the microenvironment. Taken together, we have uncovered a novel tumor suppressive function of miR-155 in the tumor microenvironment, which is also dependent on miR-155 expression in the tumor cells. Because of the oncogenic as well as tumor suppressive roles of miR-155, our findings warrant caution against a systemic inhibition of miR-155 for anticancer therapy.

Indexed as

MicroRNAsAnimalsCCAAT-Enhancer-Binding Protein-betaFemaleGene Knockdown TechniquesMammary Neoplasms, ExperimentalMiceMice, Mutant StrainsMyeloid-Derived Suppressor CellsOncogenesTumor MicroenvironmentCCAAT-Enhancer-Binding Protein-betaMicroRNAsMirn155 microRNA, mousebreast cancerC/EBP-betacytokineMDSCmiR-155

Identifiers

PMID26848978
PMCPMC4905460
OpenAlexW2293218171

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.