Evidence map›Paper›PMID 26468017›Full record

ArticleTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine2016

Down-expression of miR-152 lead to impaired anti-tumor effect of NK via upregulation of HLA-G.

Xiaokun Bian, Yuanquan Si, Min Zhang, Ran Wei, Xiaomin Yang, Hao Ren, Guixi Zheng, Chuanxin Wang, Yi Zhang

Abstract read
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In one paragraph

Article in Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.7field-weighted citation impact, top 17% 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

25 citing papers in PubMed, 38 citations in OpenAlex.

  1. Emerging Immune-Based Therapeutic Strategies in Hepatocellular Carcinoma.Liver international : official journal of the International Association for the Study of the Liver · 2026
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  13. Role of HLA-G in Viral Infections.Frontiers in immunology · 2022
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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

9 authors at 2 institutions in 1 country.

Xiaokun BianDepartment of Clinical Laboratory, Qilu Hospital of Shandong University, Jinan, China.
Yuanquan SiDepartment of Clinical Laboratory, Qilu Hospital of Shandong University, Jinan, China.
Min ZhangDepartment of Medicine, Shandong Provincial Chest Hospital, Jinan, China.
Ran WeiDepartment of Clinical Laboratory, Qilu Hospital of Shandong University, Jinan, China.
Xiaomin YangDepartment of Clinical Laboratory, Qilu Hospital of Shandong University, Jinan, China.
Hao RenDepartment of Clinical Laboratory, Qilu Hospital of Shandong University, Jinan, China.
Guixi ZhengDepartment of Clinical Laboratory, Qilu Hospital of Shandong University, Jinan, China.
Chuanxin WangDepartment of Clinical Laboratory, Qilu Hospital of Shandong University, Jinan, China.
Yi ZhangDepartment of Clinical Laboratory, Qilu Hospital of Shandong University, Jinan, China. yizhang@sdu.edu.cn.
Qilu Hospital of Shandong University · CNShandong Chest Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

It is known that chronic HBV infection (CHB) is the major risk factor for hepatocellular carcinoma (HCC) because CHB could not only cause liver tumorigenesis but also lead to change of local microenviroment and lower immune response to infected and cancerous cells (immune tolerance). Human leucocyte antigen-G (HLA-G) belongs to a non-classic MHC-I family and was considered to be an immune tolerance molecule, which could bind to immunosuppressive receptors of natural killer cell (NK) and T cells and trigger immunosuppressive signaling. Recently, numerous studies highlighted that microRNAs (miRNAs) were significantly differentially expressed in HCC tumorigenesis, and the expression was tissue-specific, indicating that miRNAs may cause great epigenetic changes in HCC tumorigenesis. In this study, we found that the expression of HLA-G was upregulated by hepatitis B virus (HBV) infection and miR-152; a HLA-G-targeting miRNA was downregulated by HBV infection. And high expression of HLA-G further suppressed NK against cancer cells, providing a new concept that miR-152 was involved in HBV-induced hepatocellular carcinoma.

Indexed as

Gene Expression Regulation, NeoplasticAdultAgedBlotting, WesternCarcinoma, HepatocellularDown-RegulationHepatitis B, ChronicHepatitis B virusHep G2 CellsHLA-G AntigensHost-Pathogen InteractionsHumansKiller Cells, NaturalLiver NeoplasmsMaleMicroRNAsHLA-G AntigensMicroRNAsMIRN152 microRNA, humanHBVHLA-GImmune tolerancemiR-152

Identifiers

PMID26468017
OpenAlexW1951233870

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.