Evidence map›Paper›PMID 28990231›Full record

ArticleCell proliferation2017

IFI16 restoration in hepatocellular carcinoma induces tumour inhibition via activation of p53 signals and inflammasome.

Wei Lin, Zhiguang Zhao, Zhonglin Ni, Yaxin Zhao, Wenjun Du, Shijun Chen

Abstract read
In one paragraph

Article in Cell proliferation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

26 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  3. Review
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  7. Molecular Mechanisms of IL18 in Disease.International journal of molecular sciences · 2023
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  8. Cells · 2023
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  9. Review
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  11. DNA and RNA Binding Proteins: From Motifs to Roles in Cancer.International journal of molecular sciences · 2022
    Review
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  13. Article
  14. Pyroptosis: mechanisms and diseases.Signal transduction and targeted therapy · 2021
    Review
  15. Article
  16. Frontiers in genetics · 2021
    Article
  17. Review
  18. Article
  19. Article
  20. Article
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.

Wei LinShandong University School of Medicine, Jinan, Shandong, China.
Zhiguang ZhaoDepartment of Pathology, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, China.
Zhonglin NiDepartment of General Surgery, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, China.
Yaxin ZhaoDepartment of Breast Surgery, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, China.
Wenjun DuDigestive Department, Shandong Provincial Qianfoshan Hospital, Shandong University, Jinan, Shandong, China.ORCID http://orcid.org/0000-0001-6214-0429
Shijun ChenDepartment of Liver Disease, Jinan Infectious Disease Hospital, Shandong University, Jinan, Shandong, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveInterferon-inducible 16 (IFI16) is known to involve in p53-dependent tumour suppression and also the formation of inflammasome, which function, however, remains controversy during carcinogenesis as a pattern recognition receptor for tumour death-derived free DNA. In this study, we investigated the anti-tumour role of IFI16 in hepatocellular carcinoma (HCC). MATERIALS AND

methodsHepatocellular carcinoma tissues (n = 20) and corresponding non-neoplastic tissues (n = 20) were collected to determine the expression of IFI16. After the transfection of pcDNA3.1-IFI16 into Huh7 and SMMC7721 cells in vitro, the influence of IFI16 overexpression on cell vitality, colony formation, apoptosis and migration were analysed. The role effect of IFI16 in vivo was further investigated.

resultsThe expression of IFI16 was significantly decreased in tumour tissues and cell lines. Overexpression of IFI16 induced decrease of cell vitality, colony formation and increased apoptosis with impaired ability of migration. Mechanistically, IFI16 could activate p53 at Ser15 to up-regulate the p21

conclusionIFI16 is a tumour suppressor in HCC via activation of p53 signals and inflammasome.

Indexed as

BenzothiazolesCarcinoma, HepatocellularCell LineHumansInflammasomesLiver NeoplasmsNuclear ProteinsPhosphoproteinsTolueneTranscriptional ActivationTumor Suppressor Protein p53BenzothiazolesIFI16 protein, humanInflammasomesNuclear ProteinsPhosphoproteinspifithrinTolueneTP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID28990231
PMCPMC6529087

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.