Evidence map›Paper›PMID 28550492›Full record

ArticleCytotechnology2018

microRNA-889 is downregulated by histone deacetylase inhibitors and confers resistance to natural killer cytotoxicity in hepatocellular carcinoma cells.

Haitao Xie, Qiugui Zhang, Hui Zhou, Jun Zhou, Ji Zhang, Yan Jiang, Jinghong Wang, Xianglin Meng, Leping Zeng, Xiaoxin Jiang

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cytotechnology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.9field-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

21 citing papers in PubMed, 31 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

10 authors at 4 institutions in 1 country.

Haitao XieDepartment of Clinical Laboratory, The First Affiliated Hospital, University of South China, Hengyang, China.
Qiugui ZhangDepartment of Clinical Laboratory, The First Affiliated Hospital, University of South China, Hengyang, China.
Hui ZhouTumor Hospital Xiangya School of Medicine of Central South University, Changsha, China.
Jun ZhouDepartment of Rehabilitation, The First Affiliated Hospital, University of South China, Hengyang, China.
Ji ZhangLaboratory of Rheumatology and Immunology, The First Affiliated Hospital, University of South China, Hengyang, China.
Yan JiangDepartment of Clinical Laboratory, The First Affiliated Hospital, University of South China, Hengyang, China.
Jinghong WangDepartment of Clinical Laboratory, The First Affiliated Hospital, University of South China, Hengyang, China.
Xianglin MengDepartment of Clinical Laboratory, The First Affiliated Hospital, University of South China, Hengyang, China.
Leping ZengDepartment of Anatomy and Neurobiology, Biology Postdoctoral Workstation, Basic School of Medicine, Central South University, Changsha, China. zengleping@hotmail.com.
Xiaoxin JiangDepartment of Clinical Laboratory, The First Affiliated Hospital, University of South China, Hengyang, China. tYHu4321568@163.com.
University of South China · CNFirst Affiliated Hospital of University of South China · CNCentral South University · CNXiangya Hospital Central South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Major histocompatibility complex class I chain-related gene B (MICB) is expressed on tumor cells and participates in natural killer (NK) cell-mediated antitumor immune response through engagement with the NKG2D receptor. This study was undertaken to identify novel microRNA (miRNA) regulators of MICB and clarify their functions in NK cell-mediated cytotoxicity to hepatocellular carcinoma (HCC) cells. Bioinformatic analysis and luciferase reporter assay were conducted to search for MICB-targeting miRNAs. Overexpression and knockdown experiments were performed to determine the roles of candidate miRNAs in the susceptibility of HCC cells to NK lysis. miR-889 was identified as a novel MICB-targeting miRNA and overexpression of miR-889 significantly inhibited the mRNA and protein expression of MICB in HepG2 and SMMC7721 HCC cells. miR-889 expression had a negative correlation with MICB mRNA levels in HCC specimens (r = -0.392, P = 0.0146). NK cell-mediated cytotoxicity was reduced in miR-889-overexpressing HCC cells, which was reversed by restoration of MICB expression. In contrast, knockdown of miR-889 led to more pronounced NK cell-mediated lysis in HCC cells. HCC cells exposed to the histone deacetylase (HDAC) inhibitor sodium valproate showed downregulation of miR-889. Enforced expression of miR-889 prevented the upregulation of MICB and enhancement of NK cell-mediated lysis by HDAC inhibitors. In conclusion, miR-889 upregulation attenuates the susceptibility of HCC cells to NK lysis and represents a potential target for improving NK cell-based antitumor therapies.

Indexed as

Hepatocellular carcinomaImmune escapemicroRNANatural killer cellsTarget gene

Identifiers

PMID28550492
PMCPMC5851948
OpenAlexW2619104463

What OpenQuestion holds

Textmetadata
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.