Evidence map›Paper›PMID 25826780›Full record

ArticleScientific reports2015

MicroRNA profiling of CD3+ CD56+ cytokine-induced killer cells.

Wenju Wang, Ruhong Li, Mingyao Meng, Chuanyu Wei, Yanhua Xie, Yayong Zhang, Lihong Jiang, Ruiyi Dong, Chunhui Wang, Yiming Zhong and 5 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.4field-weighted citation impact, top 37% 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

7 citing papers in PubMed, 10 citations in OpenAlex.

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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

15 authors at 2 institutions in 1 country.

Wenju Wang1] Yan'an Affiliated Hospital of Kunming Medical University, Kunming 650051, Yunnan, People's Republic of China [2] Yunnan Cell Biology and Clinical Translation Research Center, Kunming 650051, Yunnan, People's Republic of China.
Ruhong Li1] Yan'an Affiliated Hospital of Kunming Medical University, Kunming 650051, Yunnan, People's Republic of China [2] Yunnan Cell Biology and Clinical Translation Research Center, Kunming 650051, Yunnan, People's Republic of China.
Mingyao Meng1] Yan'an Affiliated Hospital of Kunming Medical University, Kunming 650051, Yunnan, People's Republic of China [2] Yunnan Cell Biology and Clinical Translation Research Center, Kunming 650051, Yunnan, People's Republic of China.
Chuanyu Wei1] Yan'an Affiliated Hospital of Kunming Medical University, Kunming 650051, Yunnan, People's Republic of China [2] Yunnan Cell Biology and Clinical Translation Research Center, Kunming 650051, Yunnan, People's Republic of China.
Yanhua Xie1] Yan'an Affiliated Hospital of Kunming Medical University, Kunming 650051, Yunnan, People's Republic of China [2] Yunnan Cell Biology and Clinical Translation Research Center, Kunming 650051, Yunnan, People's Republic of China.
Yayong ZhangYan'an Affiliated Hospital of Kunming Medical University, Kunming 650051, Yunnan, People's Republic of China.
Lihong JiangYan'an Affiliated Hospital of Kunming Medical University, Kunming 650051, Yunnan, People's Republic of China.
Ruiyi Dong1] Yan'an Affiliated Hospital of Kunming Medical University, Kunming 650051, Yunnan, People's Republic of China [2] Yunnan Cell Biology and Clinical Translation Research Center, Kunming 650051, Yunnan, People's Republic of China.
Chunhui Wang1] Yan'an Affiliated Hospital of Kunming Medical University, Kunming 650051, Yunnan, People's Republic of China [2] Yunnan Cell Biology and Clinical Translation Research Center, Kunming 650051, Yunnan, People's Republic of China.
Yiming Zhong1] Yan'an Affiliated Hospital of Kunming Medical University, Kunming 650051, Yunnan, People's Republic of China [2] Yunnan Cell Biology and Clinical Translation Research Center, Kunming 650051, Yunnan, People's Republic of China.
Fang Yang1] Yunnan Cell Biology and Clinical Translation Research Center, Kunming 650051, Yunnan, People's Republic of China [2] Kunming Medical University, Kunming 650050, Yunnan, People's Republic of China.
Weiwei Tang1] Yan'an Affiliated Hospital of Kunming Medical University, Kunming 650051, Yunnan, People's Republic of China [2] Yunnan Cell Biology and Clinical Translation Research Center, Kunming 650051, Yunnan, People's Republic of China.
Xingfang Jin1] Yan'an Affiliated Hospital of Kunming Medical University, Kunming 650051, Yunnan, People's Republic of China [2] Yunnan Cell Biology and Clinical Translation Research Center, Kunming 650051, Yunnan, People's Republic of China.
Baohua LiuKunming Medical University, Kunming 650050, Yunnan, People's Republic of China.
Zongliu Hou1] Yan'an Affiliated Hospital of Kunming Medical University, Kunming 650051, Yunnan, People's Republic of China [2] Yunnan Cell Biology and Clinical Translation Research Center, Kunming 650051, Yunnan, People's Republic of China.
Kunming Medical University · CNYan'an Hospital Affiliated To Kunming Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Studies have proven that IL-2 and IL-15 showed contrasting roles during CIK cells preparation. By employing microarray, we analyzed miRNA expression profiles of PBMC, CIKIL-2 and CIKIL-15. Advanced bioinformatic analyses were performed to explore the key miRNAs which may regulate cell proliferation and anti-tumor activity of CIK. We identified 261 differentially expressed miRNAs (DEMs) between PBMC and CIKIL-2, and 249 DEMs between PBMC and CIKIL-15. MiR-143-3p/miR-145-5p was miRNA cluster which may positively regulate cell proliferation. In contrast, miR-340-5p/miR-340-3p cluster may negatively regulate cell proliferation via induction apoptosis, which may cause decreased cell proliferation capacity of CIKIL-2. MiRNA-target interaction analysis indicated that 10 co-downregulated miRNAs may synergistically turn on the expression of a pool of tumor cytotoxic genes in CIK cells. The DEMs between CIKIL-2 and CIKIL-15 may contribute to enhanced tumor cytotoxic capacity of CIKIL-2. Importantly, we found that repressed miR-193a-5p may regulate the expressions of inhibitory receptor KLRD1. The results of the validation assay have shown that KLRD1 were upregulated in CIK cells. Our findings have provided new insights into mechanisms of CIK cells production and tumor cytotoxic function, and shed light on their safety for clinical trial.

Indexed as

Gene Expression ProfilingTranscriptomeCD3 ComplexCD56 AntigenChromosome MappingCluster AnalysisCytokine-Induced Killer CellsCytotoxicity, ImmunologicGene Expression RegulationGene OntologyGene Regulatory NetworksHumansImmunophenotypingLeukocytes, MononuclearMicroRNAsNeoplasmsCD3 ComplexCD56 AntigenMicroRNAsRNA, Messenger

Identifiers

PMID25826780
PMCPMC5380330
OpenAlexW1971021844

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.