Evidence map›Paper›PMID 36104978›Full record

ArticleCancer science2023

AIM2 upregulation promotes metastatic progression and PD-L1 expression in lung adenocarcinoma.

Jing-Quan Zheng, Che-Hsuan Lin, Hsun-Hua Lee, Wei-Ming Chang, Li-Jie Li, Chia-Yi Su, Kang-Yun Lee, Hui-Wen Chiu, Yuan-Feng Lin

Open access · goldAbstract read
In one paragraph

Article in Cancer science, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.4field-weighted citation impact, top 9% 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

20 citing papers in PubMed, 26 citations in OpenAlex.

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  18. The role of AIM2 in inflammation and tumors.Frontiers in immunology · 2024
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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 4 institutions in 2 countries.

Jing-Quan ZhengGraduate Institute of Clinical Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan.
Che-Hsuan LinDepartment of Otolaryngology, Taipei Medical University Hospital, Taipei Medical University, Taipei, Taiwan.
Hsun-Hua LeeDepartment of Neurology, Taipei Medical University Hospital, Taipei Medical University, Taipei, Taiwan.
Wei-Ming ChangSchool of Oral Hygiene, College of Oral Medicine, Taipei Medical University, Taipei, Taiwan.ORCID https://orcid.org/0000-0002-6899-4043
Li-Jie LiPh.D. Program of School of Dentistry, College of Oral Medicine, Taipei Medical University, Taipei, Taiwan.
Chia-Yi SuDepartment of Pharmacology, University of Minnesota Medical School, Minneapolis, Minnesota, USA.
Kang-Yun LeeGraduate Institute of Clinical Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan.
Hui-Wen ChiuGraduate Institute of Clinical Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan.ORCID https://orcid.org/0000-0002-5027-390X
Yuan-Feng LinGraduate Institute of Clinical Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan.ORCID https://orcid.org/0000-0003-4456-0766
Taipei Medical University Hospital · TWTaipei Medical University-Shuang Ho Hospital · TWTaipei Medical University · TWUniversity of Minnesota Medical Center · US

Funding

Ministry of Science and Technology, Taiwan MOST 108-2314-B-038-016Ministry of Science and Technology, Taiwan MOST 108-2320-B-038-017-MY3
6 · The paper itself

Abstract

Cancer metastasis leading to the dysfunction of invaded organs is the main cause of the reduced survival rates in lung cancer patients. However, the molecular mechanism for lung cancer metastasis remains unclear. Recently, the increased activity of inflammasome appeared to correlate with the metastatic progression and immunosuppressive ability of various cancer types. Our results showed that the mRNA levels of absence in melanoma 2 (AIM2), one of the inflammasome members, are extensively upregulated in primary tumors compared with normal tissues derived from the TCGA lung adenocarcinoma (LUAD) database. Moreover, Kaplan-Meier analysis demonstrated that a higher mRNA level of AIM2 refers to a poor prognosis in LUAD patients. Particularly, AIM2 upregulation is closely correlated with smoking history and the absence of EGFR/KRAS/ALK mutations in LUAD. We further showed that the endogenous mRNA levels of AIM2 are causally associated with the metastatic potentials of the tested LUAD cell lines. AIM2 knockdown suppressed but overexpression promoted the migration ability and lung colony-forming ability of tested LUAD cells. In addition, we found that AIM2 upregulation is closely associated with an increased level of immune checkpoint gene set, as well as programmed cell death-ligand 1 (PD-L1) transcript, in TCGA LUAD samples. AIM2 knockdown predominantly repressed but overexpression enhanced PD-L1 expression via altering the activity of PD-L1 transcriptional regulators NF-κB/STAT1 in LUAD cells. Our results not only provide a possible mechanism underlying the AIM2-promoted metastatic progression and immune evasion of LUAD but also offer a new strategy for combating metastatic/immunosuppressive LUAD via targeting AIM2 activity.

Indexed as

Adenocarcinoma of LungLung NeoplasmsMelanomaB7-H1 AntigenDNA-Binding ProteinsHumansInflammasomesPrognosisRNA, MessengerUp-RegulationAIM2 protein, humanB7-H1 AntigenDNA-Binding ProteinsInflammasomesRNA, MessengerAIM2 inflammasomecancer metastasisepithelial-mesenchymal transitionlung cancerPD-L1

Identifiers

PMID36104978
PMCPMC9807530
OpenAlexW4295901331

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.