Evidence map›Paper›PMID 38170337›Full record

ArticleDigestive diseases and sciences2024

Interferon-Gamma-Inducible Protein 16 Inhibits Hepatocellular Carcinoma via Interferon Regulatory Factor 3 on Chemosensitivity.

Wei Lin, Zhiguang Zhao, Wenjun Du, Zhonglin Ni, Chenwei Pan, Peipei Fang, Jie Li, Lu ZhuGe, Shuanghong Jin

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Article in Digestive diseases and sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.5field-weighted citation impact, top 39% 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

2 citing papers in PubMed, 2 citations in OpenAlex.

  1. Article
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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 1 institution in 1 country.

Wei Lin *Department of Infectious Diseases, The Second Affiliated Hospital of Wenzhou Medical University, #1111 of Wenzhou Wenzhou Avenue, Longwan District, Wenzhou, Zhejiang, China. linwei01@wmu.edu.cn.ORCID http://orcid.org/0009-0006-4406-3830
Zhiguang Zhao *Department of Pathology, The Second Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, China.
Wenjun Du *Department of Liver Diseases, Shandong Public Health Clinical Center, Shangdong University, Jinan, Shangdong, China.
Zhonglin Ni *Department of Hepatobiliary and Pancreatic Surgery, The Second Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, China.
Chenwei PanDepartment of Infectious Diseases, The Second Affiliated Hospital of Wenzhou Medical University, #1111 of Wenzhou Wenzhou Avenue, Longwan District, Wenzhou, Zhejiang, China.
Peipei FangDepartment of Infectious Diseases, The Second Affiliated Hospital of Wenzhou Medical University, #1111 of Wenzhou Wenzhou Avenue, Longwan District, Wenzhou, Zhejiang, China.
Jie LiDepartment of Infectious Diseases, The Second Affiliated Hospital of Wenzhou Medical University, #1111 of Wenzhou Wenzhou Avenue, Longwan District, Wenzhou, Zhejiang, China.
Lu ZhuGeDepartment of Infectious Diseases, The Second Affiliated Hospital of Wenzhou Medical University, #1111 of Wenzhou Wenzhou Avenue, Longwan District, Wenzhou, Zhejiang, China.
Shuanghong JinDepartment of Infectious Diseases, The Second Affiliated Hospital of Wenzhou Medical University, #1111 of Wenzhou Wenzhou Avenue, Longwan District, Wenzhou, Zhejiang, China.
Wenzhou Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND AND

aimPrevious reports have suggested IFI16 as a tumor suppressor in hepatocellular carcinoma (HC). Nonetheless, the biological significance of IFI16 and its mechanism concerning resistance to cisplatin (DDP) in HC requires further exploration.

methodsSamples of tumor and corresponding para-carcinoma tissues were acquired from patients with HC. Furthermore, DDP-resistant cell lines of HC, specifically HCC, Huh7 and Hepatoblastoma, HepG3, were generated by gradually increasing the concentration of DDP. Cell apoptosis and DNA damage were evaluated by utilizing flow cytometry assay and TUNEL staining. The interaction between IFI16 and interferon regulatory factor 3 (IRF3) proteins were analyzed using Co-Immunoprecipitation (Co-IP) assay. In vivo assays were conducted by establishing HC subcutaneous xenograft tumor models.

resultsThe study found a reduction in IFI16 expression in both HC tissues and DDP-resistant HC cell lines. The binding of IFI16 to IRF3 regulated DNA damage-associated markers in vitro. Overexpression of IFI16 heightened the susceptibility of DDP-induced apoptosis and DNA damage, which was counteracted by IRF3 knockdown, while strengthened by IRF3 overexpression. Moreover, overexpression of IFI16 diminished in vivo DDP-resistant HC tumorigenicity.

conclusionIn summary, our findings suggest that IFI16 serves as a tumor suppressor in HC by promoting DNA damage via its interaction with IRF3, thereby reversing DDP resistance.

Indexed as

Carcinoma, HepatocellularLiver NeoplasmsMicroRNAsCell Line, TumorCell ProliferationCisplatinDrug Resistance, NeoplasmHumansInterferon-gammaInterferon Regulatory Factor-3CisplatinInterferon-gammaInterferon Regulatory Factor-3MicroRNAsDDP resistanceDNA damageIFI16IRF3Liver cancer

Identifiers

PMID38170337
OpenAlexW4390546461

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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.