Evidence map›Paper›PMID 29067466›Full record

ArticleMolecular medicine reports2017

miR-128 enhances dendritic cell-mediated anti-tumor immunity via targeting of p38.

Xue Liang, Wenfeng Shangguan, Miaomiao Zhang, Shiyue Mei, Liyang Wang, Rongcun Yang

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 1 pooled it
0.6field-weighted citation impact, top 36% 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

12 citing papers in PubMed, 1 synthesis or guideline pooled it, 19 citations in OpenAlex.

  1. The Roles of MiRNAs (MicroRNAs) in Melanoma Immunotherapy.International journal of molecular sciences · 2022
    Pooled it
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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

6 authors at 4 institutions in 2 countries.

Xue LiangDepartment of Cardiology, Tianjin Key Laboratory of Ionic‑Molecular Function of Cardiovascular Disease, Tianjin Institute of Cardiology, Second Hospital of Tianjin Medical University, Tianjin 300211, P.R. China.
Wenfeng ShangguanDepartment of Cardiology, Tianjin Key Laboratory of Ionic‑Molecular Function of Cardiovascular Disease, Tianjin Institute of Cardiology, Second Hospital of Tianjin Medical University, Tianjin 300211, P.R. China.
Miaomiao ZhangState Key Laboratory of Medicinal Chemical Biology, School of Medicine, Nankai University, Tianjin 300071, P.R. China.
Shiyue MeiState Key Laboratory of Medicinal Chemical Biology, School of Medicine, Nankai University, Tianjin 300071, P.R. China.
Liyang WangFaculty of Medicine, University of Southampton, Southampton, Hampshire SO17 1BJ, UK.
Rongcun YangState Key Laboratory of Medicinal Chemical Biology, School of Medicine, Nankai University, Tianjin 300071, P.R. China.
Nankai University · CNSecond Hospital of Tianjin Medical University · CNTianjin Medical University · CNUniversity of Southampton · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

MiRNA (miR)-128, which is a well‑recognized inhibitor of tumor growth, is involved in the anti-tumor function of dendritic cells (DCs). However, the association between miR‑128 and the DC‑mediated anti‑tumor immunity remains to be elucidated. Murine B16 melanoma cells and C57BL/6 male mice were used to obtain marrow‑derived DCs. DCs were treated with B16 cell suspension. miR‑128 mimic, miR‑128 inhibitor, p38 inhibitor or negative control oligonucleotides were transfected into DCs. After transfection, mRNA and protein expression of p38 in DCs was detected via reverse transcription‑quantitative polymerase chain reaction and western blotting. The present study demonstrated that the miR‑128 abundance in DCs was significantly attenuated by B16 (a melanoma cell line) stimulation and the protein expression level of p38 was increased. Additionally, miR‑128 inhibited the protein expression of p38 in DCs in a dose‑dependent manner, however no significant effect on the p38 mRNA level was observed. Furthermore, miR‑128 mimic or p38 inhibitor decreased the mRNA expression and secretion of interleukin (IL)‑6 and IL‑10 cytokines and increased the level of IL‑12 in DCs, whereas an miR‑128 inhibitor exhibited the opposite effects. These findings suggested that miR‑128 regulated the immune response of DCs via p38‑downstream cytokines. Furthermore, the tumor growth rate, size and weight were markedly decreased and the survival time prolonged, following injection of DCs harboring miR‑128 mimic or p38 inhibitor in C57BL/6 mice bearing B16 melanoma. The results therefore suggest that miR‑128 enhances the anti‑tumor immunity response of DCs via targeting of the p38 mitogen activated protein kinase signaling pathway.

Indexed as

AnimalsAntagomirsDendritic CellsEnzyme-Linked Immunosorbent AssayImmunity, CellularInterleukin-10Interleukin-12Interleukin-6MaleMelanoma, ExperimentalMiceMice, Inbred C57BLMicroRNAsp38 Mitogen-Activated Protein KinasesRNA InterferenceRNA, Small InterferingAntagomirsInterleukin-10Interleukin-12Interleukin-6MicroRNAsMirn128 microRNA, mousep38 Mitogen-Activated Protein KinasesRNA, Small Interfering

Identifiers

PMID29067466
PMCPMC5561786
OpenAlexW2623983485

What OpenQuestion holds

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LicenceCC BY-NC-ND
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.