Evidence map›Paper›PMID 23221562›Full record

ArticleJournal of virology2013

Hepatitis B virus mRNA-mediated miR-122 inhibition upregulates PTTG1-binding protein, which promotes hepatocellular carcinoma tumor growth and cell invasion.

Changfei Li, Yanzhong Wang, Saifeng Wang, Bo Wu, Junli Hao, Hongxia Fan, Ying Ju, Yuping Ding, Lizhao Chen, Xiaoyu Chu and 3 more

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

Article in Journal of virology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers.

0numbers the graph read from it
0cells of the map it votes in
85citing papers in PubMed
6.1field-weighted citation impact, top 3% 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

85 citing papers in PubMed, 146 citations in OpenAlex.

  1. MicroRNA-122 as a regulator and biomarker of liver disease.Journal of molecular medicine (Berlin, Germany) · 2026
    Review
  2. Review
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  5. Transcriptionally distinct malignant neuroblastoma populations show selective response to adavosertib treatment.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025
    Article
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  7. Review
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  9. Article
  10. Article
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  12. Cytokines and microRNAs in SARS-CoV-2: What do we know?Molecular therapy. Nucleic acids · 2022
    Review
  13. Review
  14. Review
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review

25 more citing papers are in PubMed but not listed here.

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

13 authors at 3 institutions in 1 country.

Changfei LiCAS Key Laboratory of Pathogenic Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences (CAS), Beijing, China.
Yanzhong Wang
Saifeng Wang
Bo Wu
Junli Hao
Hongxia Fan
Ying Ju
Yuping Ding
Lizhao Chen
Xiaoyu Chu
Wenjun Liu
Xin Ye
Songdong Meng
Chinese Academy of Sciences · CNInstitute of Microbiology · CNYantai Infectious Diseases Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

As the most abundant liver-specific microRNA, miR-122 is involved in diverse aspects of hepatic function and neoplastic transformation. Our previous study showed that miR-122 levels are significantly decreased in hepatitis B virus (HBV)-infected patients, which may facilitate viral replication and persistence (S. Wang, L. Qiu, X. Yan, W. Jin, Y. Wang, L. Chen, E. Wu, X. Ye, G. F. Gao, F. Wang, Y. Chen, Z. Duan, and S. Meng, Hepatology 55:730-741, 2012). Loss of miR-122 expression in patients with hepatitis B enhances hepatitis B virus replication through cyclin G1-modulated P53 activity.). In this study, we provide evidence that all HBV mRNAs harboring an miR-122 complementary site act as sponges to bind and sequester endogenous miR-122, indicating that the highly redundant HBV transcripts are involved in HBV-mediated miR-122 suppression. We next identified pituitary tumor-transforming gene 1 (PTTG1) binding factor (PBF) as a target of miR-122 and demonstrated that HBV replication causes an obvious increase in PBF levels. Furthermore, we observed that the miR-122 levels were decreased and PBF was upregulated in chronic hepatitis B (CHB) and hepatocellular carcinoma (HCC). Overexpression and knockdown studies both revealed that PBF enhances proliferation and invasion of HCC cells, and silencing PBF resulted in a dramatic reduction of HCC tumor growth in vivo. Mechanistic analysis demonstrated that PBF interacts with PTTG1 and facilitates PTTG1 nuclear translocation, subsequently increasing its transcriptional activities. Therefore, we identified a novel HBV mRNA-miR-122-PBF regulatory pathway that facilitates malignant hepatocyte growth and invasion in CHB which may contribute to CHB-induced HCC development and progression. Our work underscores the reciprocal interplay of host miRNA sequestration and depletion by viral mRNAs, which may contribute to chronic-infection-related cancer.

Indexed as

AdultAgedAnimalsCarcinoma, HepatocellularFemaleHepatitis B, ChronicHepatitis B virusHumansIntracellular Signaling Peptides and ProteinsLiver NeoplasmsMaleMembrane ProteinsMiceMice, Inbred BALB CMicroRNAsMiddle AgedIntracellular Signaling Peptides and ProteinsMembrane ProteinsMicroRNAsMIRN122 microRNA, humanPTTG1IP protein, humanRNA, MessengerRNA, Viral

Identifiers

PMID23221562
PMCPMC3571498
OpenAlexW2024175254

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.