AIM2 upregulation promotes metastatic progression and PD‐L1 expression in lung adenocarcinoma
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 metasta...
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| Published in | Cancer science Vol. 114; no. 1; pp. 306 - 320 |
|---|---|
| Main Authors | , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
England
John Wiley & Sons, Inc
01.01.2023
John Wiley and Sons Inc |
| Subjects | |
| Online Access | Get full text |
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| 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.
The illustration of a possible mechanism for the AIM2‐fostered EMT progression and PD‐L1 expression in the metastatic/immunosuppressive lung adenocarcinoma. AIM2 increases PD‐L1 expression via activating its transcriptional regulators NF‐kB/STAT1. |
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| AbstractList | 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. 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.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. 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. The illustration of a possible mechanism for the AIM2‐fostered EMT progression and PD‐L1 expression in the metastatic/immunosuppressive lung adenocarcinoma. AIM2 increases PD‐L1 expression via activating its transcriptional regulators NF‐kB/STAT1. 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. 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. The illustration of a possible mechanism for the AIM2‐fostered EMT progression and PD‐L1 expression in the metastatic/immunosuppressive lung adenocarcinoma. AIM2 increases PD‐L1 expression via activating its transcriptional regulators NF‐kB/STAT1. |
| Audience | Academic |
| Author | Chang, Wei‐Ming Li, Li‐Jie Lee, Hsun‐Hua Chiu, Hui‐Wen Su, Chia‐Yi Lin, Yuan‐Feng Lin, Che‐Hsuan Lee, Kang‐Yun Zheng, Jing‐Quan |
| AuthorAffiliation | 1 Graduate Institute of Clinical Medicine, College of Medicine Taipei Medical University Taipei Taiwan 13 TMU Research Center of Urology and Kidney Taipei Medical University Taipei Taiwan 7 Department of Neurology, School of Medicine, College of Medicine Taipei Medical University Taipei Taiwan 3 Division of Pulmonary Medicine, Department of Internal Medicine, School of Medicine, College of Medicine Taipei Medical University Taipei Taiwan 8 Dizziness and Balance Disorder Center, Shuang Ho Hospital Taipei Medical University New Taipei City Taiwan 9 School of Oral Hygiene, College of Oral Medicine Taipei Medical University Taipei Taiwan 4 Department of Otolaryngology, Taipei Medical University Hospital Taipei Medical University Taipei Taiwan 5 Department of Otolaryngology, School of Medicine, College of Medicine Taipei Medical University Taipei Taiwan 11 Department of Pharmacology University of Minnesota Medical School Minneapolis Minnesota USA 12 Department of Medical Research, Shuang Ho Hospital |
| AuthorAffiliation_xml | – name: 13 TMU Research Center of Urology and Kidney Taipei Medical University Taipei Taiwan – name: 11 Department of Pharmacology University of Minnesota Medical School Minneapolis Minnesota USA – name: 3 Division of Pulmonary Medicine, Department of Internal Medicine, School of Medicine, College of Medicine Taipei Medical University Taipei Taiwan – name: 9 School of Oral Hygiene, College of Oral Medicine Taipei Medical University Taipei Taiwan – name: 8 Dizziness and Balance Disorder Center, Shuang Ho Hospital Taipei Medical University New Taipei City Taiwan – name: 4 Department of Otolaryngology, Taipei Medical University Hospital Taipei Medical University Taipei Taiwan – name: 1 Graduate Institute of Clinical Medicine, College of Medicine Taipei Medical University Taipei Taiwan – name: 10 Ph.D. Program of School of Dentistry, College of Oral Medicine Taipei Medical University Taipei Taiwan – name: 12 Department of Medical Research, Shuang Ho Hospital Taipei Medical University New Taipei City Taiwan – name: 2 Division of Pulmonary Medicine, Department of Internal Medicine, Shuang Ho Hospital Taipei Medical University New Taipei City Taiwan – name: 6 Department of Neurology, Taipei Medical University Hospital Taipei Medical University Taipei Taiwan – name: 7 Department of Neurology, School of Medicine, College of Medicine Taipei Medical University Taipei Taiwan – name: 14 Cell Physiology and Molecular Image Research Center, Wan Fang Hospital Taipei Medical University Taipei Taiwan – name: 5 Department of Otolaryngology, School of Medicine, College of Medicine Taipei Medical University Taipei Taiwan |
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| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/36104978$$D View this record in MEDLINE/PubMed |
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| Copyright | 2022 The Authors. published by John Wiley & Sons Australia, Ltd on behalf of Japanese Cancer Association. 2022 The Authors. Cancer Science published by John Wiley & Sons Australia, Ltd on behalf of Japanese Cancer Association. COPYRIGHT 2023 John Wiley & Sons, Inc. 2023. This work is published under http://creativecommons.org/licenses/by-nc-nd/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. |
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| Snippet | 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... |
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| SubjectTerms | Adenocarcinoma Adenocarcinoma of Lung - pathology AIM2 inflammasome Apoptosis B7-H1 Antigen - genetics B7-H1 Antigen - metabolism Breast cancer cancer metastasis Cell culture Cell death Comparative analysis DNA-Binding Proteins - genetics DNA-Binding Proteins - metabolism epithelial‐mesenchymal transition Gene expression Genomes Humans Immune checkpoint Inflammasomes Inflammasomes - metabolism Lung cancer Lung Neoplasms - pathology Medical prognosis Melanoma Metastases Metastasis Original ORIGINAL ARTICLES PD-L1 protein PD‐L1 Prognosis Proteins RNA RNA, Messenger - genetics Stat1 protein Statistical significance Tumorigenesis Tumors Up-Regulation |
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| Title | AIM2 upregulation promotes metastatic progression and PD‐L1 expression in lung adenocarcinoma |
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