Evidence map›Paper›PMID 38316697›Full record

ArticleMedical molecular morphology2024

IL-32 production from lung adenocarcinoma cells is potentially involved in immunosuppressive microenvironment.

Shukang Zhao, Lianbo Li, Yoshihiro Komohara, Eri Matsubara, Yusuke Shinchi, Ahmad Adawy, Hiromu Yano, Cheng Pan, Yukio Fujiwara, Koei Ikeda and 3 more

Abstract read
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In one paragraph

Article in Medical molecular morphology, 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
–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

2 citing papers in PubMed.

  1. Translational cancer research · 2025
    Article
  2. 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

13 authors.

Shukang ZhaoDepartment of Cell Pathology, Graduate School of Medical Sciences, Kumamoto University, 1-1-1, Honjo, Kumamoto Chuo-ku, Kumamoto, 860-8556, Japan.
Lianbo LiDepartment of Cell Pathology, Graduate School of Medical Sciences, Kumamoto University, 1-1-1, Honjo, Kumamoto Chuo-ku, Kumamoto, 860-8556, Japan.
Yoshihiro KomoharaDepartment of Cell Pathology, Graduate School of Medical Sciences, Kumamoto University, 1-1-1, Honjo, Kumamoto Chuo-ku, Kumamoto, 860-8556, Japan. ycomo@kumamoto-u.ac.jp.ORCID http://orcid.org/0000-0001-9723-0846
Eri MatsubaraDepartment of Cell Pathology, Graduate School of Medical Sciences, Kumamoto University, 1-1-1, Honjo, Kumamoto Chuo-ku, Kumamoto, 860-8556, Japan.
Yusuke ShinchiDepartment of Thoracic Surgery and Breast Surgery, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan.
Ahmad AdawyDepartment of Cell Pathology, Graduate School of Medical Sciences, Kumamoto University, 1-1-1, Honjo, Kumamoto Chuo-ku, Kumamoto, 860-8556, Japan.
Hiromu YanoDepartment of Cell Pathology, Graduate School of Medical Sciences, Kumamoto University, 1-1-1, Honjo, Kumamoto Chuo-ku, Kumamoto, 860-8556, Japan.
Cheng PanDepartment of Cell Pathology, Graduate School of Medical Sciences, Kumamoto University, 1-1-1, Honjo, Kumamoto Chuo-ku, Kumamoto, 860-8556, Japan.
Yukio FujiwaraDepartment of Cell Pathology, Graduate School of Medical Sciences, Kumamoto University, 1-1-1, Honjo, Kumamoto Chuo-ku, Kumamoto, 860-8556, Japan.
Koei IkedaDepartment of Thoracic Surgery and Breast Surgery, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan.
Shinya SuzuJoint Research Center for Human Retrovirus Infection, Kumamoto University, Kumamoto, Japan.
Taizo HibiDepartment of Pediatric Surgery and Transplantation, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan.
Makoto SuzukiDepartment of Thoracic Surgery and Breast Surgery, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan.

Funding

Japan Society for the Promotion of Science London 20H03459
6 · The paper itself

Abstract

Interleukin 32 (IL-32) is a proinflammatory cytokine secreted from several kinds of cancer cells. In the present study, we investigated the significance of IL-32 in lung adenocarcinoma by immunohistochemistry and bioinformatics analysis. IL-32 was positive in cancer cells of 21 cases (9.2%) of total 228 cases. Increased IL-32 gene expression was linked to worse clinical course in TCGA analysis, however, IL-32 expression in immunohistochemistry was not associated to clinical course in our cohort. It was also found that high IL-32 expression was seen in cases with increased lymphocyte infiltration. In vitro studies indicated that IFN-γ induced gene expression of IL-32 and PD1-ligands in lung adenocarcinoma cell lines. IL-32, especially IL-32β, also induced overexpression of PD1-ligands in human monocyte-derived macrophages. Additionally, Cancer-cell-derived IL-32 was elevated by stimulation with anticancer agents. In conclusion, IL-32 potentially induced by inflammatory conditions and anticancer therapy and contribute to immune escape of cancer cells via development the immunosuppressive microenvironment. IL-32 might be a target molecule for anti-cancer therapy.

Indexed as

Adenocarcinoma of LungInterleukinsLung NeoplasmsTumor MicroenvironmentA549 CellsCell Line, TumorGene Expression Regulation, NeoplasticHumansImmunohistochemistryInterferon-gammaMacrophagesMaleIL32 protein, humanInterferon-gammaInterleukinsAdenocarcinomaIL-32Lung cancerMacrophageTumor microenvironment

Identifiers

PMID38316697

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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.