Evidence map›Paper›PMID 25594054›Full record

ArticleOncoscience2014

MicroRNA-17 inhibits tumor growth by stimulating T-cell mediated host immune response.

Haoran Li, Shaan Gupta, William W Du, Burton B Yang

Open access · hybridAbstract read
In one paragraph

Article in Oncoscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 1 pooled it
3.0field-weighted citation impact, top 7% 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

24 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 citations in OpenAlex.

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  14. Targeting microRNAs as key modulators of tumor immune response.Journal of experimental & clinical cancer research : CR · 2016
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

4 authors at 2 institutions in 1 country.

Haoran LiSunnybrook Research Institute, Sunnybrook Health Sciences Centre, Toronto ; Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto.
Shaan GuptaSunnybrook Research Institute, Sunnybrook Health Sciences Centre, Toronto ; Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto.
William W DuSunnybrook Research Institute, Sunnybrook Health Sciences Centre, Toronto ; Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto.
Burton B YangSunnybrook Research Institute, Sunnybrook Health Sciences Centre, Toronto ; Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto.
Sunnybrook Health Science Centre · CASunnybrook Research Institute

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMelanoma is one of the fastest-rising types of cancer in North American. Accumulating evidence suggests that anti-tumor immune tolerance plays a critical role in tumor development.

methodsB16 melanoma cells were injected into wild type and miR-17 overexpressing transgenic mice. Tumor growth was monitored and tumor bearing mice were sacrificed by the end of the forth week. Peripheral blood and spleen cells were subject to flow cytometry analysis and tumor samples were subject to immunohistochemistry staining. Meanwhile, Jurkat cells transfected with mock-control or miR-17 overexpressing plasmid were co-cultured with B16 cells. The influence of miR-17 on cell cycle, proliferation and survival was evaluated.

resultsThe melanoma tumors formed in mice overexpressing miR-17 were less than that in wild type mice. In addition, the miR-17 tumors were less invasive and less angiogenic. The percentage of CD8+ T cells was suppressed in miR-17 transgenic mice before melanoma cell injection. Its level was significantly increased upon tumor grafting. More tumor infiltrating CD8+ cytotoxic T lymphocyte could be found in transgenic mice with tumor formation. Luciferase assay and protein analysis indicated that STAT3 was the target of miR-17. Decreased levels of STAT3 were associated with miR-17 over-expression. Down-regulation of STAT3 in Jurkat cells promoted cell proliferation and mitosis.

conclusionsMiR-17 inhibits melanoma growth by stimulating CD8+ T cells mediated host immune response, which is due to its regulation of STAT3.

Indexed as

immune responsemicroRNAmiR-17Stat3T-cell

Identifiers

PMID25594054
PMCPMC4278315
OpenAlexW2398392409

What OpenQuestion holds

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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.