Evidence map›Paper›PMID 26008967›Full record

ArticleOncotarget2015

MMP3-mediated tumor progression is controlled transcriptionally by a novel IRF8-MMP3 interaction.

Debarati Banik, Colleen S Netherby, Paul N Bogner, Scott I Abrams

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 1 pooled it
0.8field-weighted citation impact, top 29% 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

21 citing papers in PubMed, 1 synthesis or guideline pooled it, 53 citations in OpenAlex.

  1. Pooled it
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  6. Review
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  9. Article
  10. Beneficial effects ofToxicological research · 2021
    Article
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  14. Review
  15. MicroRNA-18a-5p Suppresses Tumor GrowthFrontiers in oncology · 2020
    Article
  16. [Research progress on interleukin-6 in lung cancer].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2018
    Review
  17. Article
  18. 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

4 authors at 1 institution in 1 country.

Debarati BanikDepartment of Immunology, Roswell Park Cancer Institute, Elm and Carlton Streets, Buffalo, NY 14263, USA.
Colleen S NetherbyDepartment of Immunology, Roswell Park Cancer Institute, Elm and Carlton Streets, Buffalo, NY 14263, USA.
Paul N BognerDepartment of Pathology, Roswell Park Cancer Institute, Elm and Carlton Streets, Buffalo, NY 14263, USA.
Scott I AbramsDepartment of Immunology, Roswell Park Cancer Institute, Elm and Carlton Streets, Buffalo, NY 14263, USA.
Roswell Park Comprehensive Cancer Center · US

Funding

Two-Spirit Films in Indigenous Cancer HealthP30CA016056 · NCI · ROSWELL PARK CANCER INSTITUTE CORP · PI MARK G FRATTINI · 1985 to 2026
$116.6M
MULTIDISCIPLINARY APPROACHES TUMOR IMMUNOLOGYT32CA085183 · NCI · ROSWELL PARK CANCER INSTITUTE CORP · PI Scott I. Abrams · 2001 to 2026
$3.1M
Mechanisms Underlying Functional Programs of Tumor-Associated MacrophagesR01CA172105 · NCI · ROSWELL PARK CANCER INSTITUTE CORP · PI ABRAMS, SCOTT I. · 2015 to 2019
$2.0M
IRF-8 as a Negative Regulator of CD11b+Gr-1+ Myeloid Cell Production and FunctionR01CA140622 · NCI · ROSWELL PARK CANCER INSTITUTE CORP · PI ABRAMS, SCOTT I. · 2011 to 2015
$2.0M
NCI NIH HHS CA016056NCI NIH HHS P30 CA016056NCI NIH HHS R01 CA140622NCI NIH HHS R01CA140622NCI NIH HHS R01 CA172105NCI NIH HHS R01CA172105NCI NIH HHS T32 CA085183NCI NIH HHS T32CA085183
6 · The paper itself

Abstract

Interferon regulatory factor-8 (IRF8), originally identified as a leukemic tumor suppressor, can also exert anti-neoplastic activities in solid tumors. We previously showed that IRF8-loss enhanced tumor growth, which was accompanied by reduced tumor-cell susceptibility to apoptosis. However, the impact of IRF8 expression on tumor growth could not be explained solely by its effects on regulating apoptotic response. Exploratory gene expression profiling further revealed an inverse relationship between IRF8 and MMP3 expression, implying additional intrinsic mechanisms by which IRF8 modulated neoplastic behavior. Although MMP3 expression was originally linked to tumor initiation, the role of MMP3 beyond this stage has remained unclear. Therefore, we hypothesized that MMP3 governed later stages of disease, including progression to metastasis, and did so through a novel IRF8-MMP3 axis. Altogether, we showed an inverse mechanistic relationship between IRF8 and MMP3 expression in tumor progression. Importantly, the growth advantage due to IRF8-loss was significantly compromised after silencing MMP3 expression. Moreover, MMP3-loss reduced spontaneous lung metastasis in an orthotopic mouse model of mammary carcinoma. MMP3 acted, in part, in a cell-intrinsic manner and served as a direct transcriptional target of IRF8. Thus, we identified a novel role of an IRF8-MMP3 axis in tumor progression, which unveils new therapeutic opportunities.

Indexed as

Gene Expression Regulation, NeoplasticAnimalsBase SequenceBlotting, WesternCell LineCell Line, TumorDisease ProgressionFemaleHumansInterferon Regulatory Factor-8Interferon Regulatory FactorsMatrix Metalloproteinase 3Mice, Inbred BALB CMice, SCIDMolecular Sequence DataNeoplasm InvasivenessInterferon Regulatory Factor-8Interferon Regulatory FactorsMatrix Metalloproteinase 3host-tumor interactioninterferon regulatory factor-8matrix metalloproteinase-3metastasistumor progression

Identifiers

PMID26008967
PMCPMC4558143
OpenAlexW1943868360

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.