Loss of GSTO2 contributes to cell growth and mitochondria function via the p38 signaling in lung squamous cell carcinoma
Glutathione S‐transferase omega 2 (GSTO2) lacks any appreciable GST activity, but it exhibits thioltransferase activity. The significance of GSTO2 in lung function has been reported; however, the precise expression and molecular function of GSTO2 in the lungs remain unclear. In the present study, we...
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| Published in | Cancer science Vol. 113; no. 1; pp. 195 - 204 |
|---|---|
| Main Authors | , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
England
John Wiley & Sons, Inc
01.01.2022
John Wiley and Sons Inc |
| Subjects | |
| Online Access | Get full text |
| ISSN | 1347-9032 1349-7006 1349-7006 |
| DOI | 10.1111/cas.15189 |
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| Abstract | Glutathione S‐transferase omega 2 (GSTO2) lacks any appreciable GST activity, but it exhibits thioltransferase activity. The significance of GSTO2 in lung function has been reported; however, the precise expression and molecular function of GSTO2 in the lungs remain unclear. In the present study, we found that GSTO2 is expressed in airway basal cells, non–ciliated, columnar Clara cells, and type II alveolar cells, which have self‐renewal capacity in the lungs. Contrastingly, no GSTO2 expression was observed in 94 lung squamous cell carcinoma (LSCC) samples. When human LSCC cell lines were treated with 5‐aza‐2′‐deoxycytidine, a DNA‐methyltransferase inhibitor, GSTO2 transcription was induced, suggesting that aberrant GSTO2 hypermethylation in LSCC is the cause of its downregulation. Forced GSTO2 expression in LSCC cell lines inhibited cell growth and colony formation in vitro. In a subcutaneous xenograft model, GSTO2‐transfected cells formed smaller tumors in nude mice than mock‐transfected cells. Upon intravenous injection into nude mice, the incidence of liver metastasis was lower in mice injected with GSTO2‐transfected cells than in those injected with mock‐transfected cells. In addition, GSTO2 induction suppressed the expression of β‐catenin and the oxygen consumption rate, but it did not affect the extracellular acidification rate. Furthermore, GSTO2‐transfected cells displayed lower mitochondrial membrane potential than mock‐transfected cells. When GSTO2‐transfected cells were treated with a p38 inhibitor, β‐catenin expression and mitochondrial membrane potential were recovered. Our study indicated that the loss of GSTO2 via DNA hypermethylation contributes to the growth and progression of LSCC, probably by modulating cancer metabolism via the p38/β‐catenin signaling pathway.
Glutathione S‐transferase omega 2 (GSTO2) is expressed in the stem cells of the bronchial and alveolar epithelium. Loss of GSTO2 might contribute to lung squamous cell carcinoma growth by modulating cancer metabolism via the p38/β‐catenin signaling pathway. |
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| AbstractList | Glutathione S‐transferase omega 2 (GSTO2) lacks any appreciable GST activity, but it exhibits thioltransferase activity. The significance of GSTO2 in lung function has been reported; however, the precise expression and molecular function of GSTO2 in the lungs remain unclear. In the present study, we found that GSTO2 is expressed in airway basal cells, non–ciliated, columnar Clara cells, and type II alveolar cells, which have self‐renewal capacity in the lungs. Contrastingly, no GSTO2 expression was observed in 94 lung squamous cell carcinoma (LSCC) samples. When human LSCC cell lines were treated with 5‐aza‐2′‐deoxycytidine, a DNA‐methyltransferase inhibitor, GSTO2 transcription was induced, suggesting that aberrant GSTO2 hypermethylation in LSCC is the cause of its downregulation. Forced GSTO2 expression in LSCC cell lines inhibited cell growth and colony formation in vitro. In a subcutaneous xenograft model, GSTO2‐transfected cells formed smaller tumors in nude mice than mock‐transfected cells. Upon intravenous injection into nude mice, the incidence of liver metastasis was lower in mice injected with GSTO2‐transfected cells than in those injected with mock‐transfected cells. In addition, GSTO2 induction suppressed the expression of β‐catenin and the oxygen consumption rate, but it did not affect the extracellular acidification rate. Furthermore, GSTO2‐transfected cells displayed lower mitochondrial membrane potential than mock‐transfected cells. When GSTO2‐transfected cells were treated with a p38 inhibitor, β‐catenin expression and mitochondrial membrane potential were recovered. Our study indicated that the loss of GSTO2 via DNA hypermethylation contributes to the growth and progression of LSCC, probably by modulating cancer metabolism via the p38/β‐catenin signaling pathway. Glutathione S‐transferase omega 2 (GSTO2) lacks any appreciable GST activity, but it exhibits thioltransferase activity. The significance of GSTO2 in lung function has been reported; however, the precise expression and molecular function of GSTO2 in the lungs remain unclear. In the present study, we found that GSTO2 is expressed in airway basal cells, non–ciliated, columnar Clara cells, and type II alveolar cells, which have self‐renewal capacity in the lungs. Contrastingly, no GSTO2 expression was observed in 94 lung squamous cell carcinoma (LSCC) samples. When human LSCC cell lines were treated with 5‐aza‐2′‐deoxycytidine, a DNA‐methyltransferase inhibitor, GSTO2 transcription was induced, suggesting that aberrant GSTO2 hypermethylation in LSCC is the cause of its downregulation. Forced GSTO2 expression in LSCC cell lines inhibited cell growth and colony formation in vitro . In a subcutaneous xenograft model, GSTO2 ‐transfected cells formed smaller tumors in nude mice than mock‐transfected cells. Upon intravenous injection into nude mice, the incidence of liver metastasis was lower in mice injected with GSTO2 ‐transfected cells than in those injected with mock‐transfected cells. In addition, GSTO2 induction suppressed the expression of β‐catenin and the oxygen consumption rate, but it did not affect the extracellular acidification rate. Furthermore, GSTO2 ‐transfected cells displayed lower mitochondrial membrane potential than mock‐transfected cells. When GSTO2 ‐transfected cells were treated with a p38 inhibitor, β‐catenin expression and mitochondrial membrane potential were recovered. Our study indicated that the loss of GSTO2 via DNA hypermethylation contributes to the growth and progression of LSCC, probably by modulating cancer metabolism via the p38/β‐catenin signaling pathway. Glutathione S‐transferase omega 2 (GSTO2) lacks any appreciable GST activity, but it exhibits thioltransferase activity. The significance of GSTO2 in lung function has been reported; however, the precise expression and molecular function of GSTO2 in the lungs remain unclear. In the present study, we found that GSTO2 is expressed in airway basal cells, non–ciliated, columnar Clara cells, and type II alveolar cells, which have self‐renewal capacity in the lungs. Contrastingly, no GSTO2 expression was observed in 94 lung squamous cell carcinoma (LSCC) samples. When human LSCC cell lines were treated with 5‐aza‐2′‐deoxycytidine, a DNA‐methyltransferase inhibitor, GSTO2 transcription was induced, suggesting that aberrant GSTO2 hypermethylation in LSCC is the cause of its downregulation. Forced GSTO2 expression in LSCC cell lines inhibited cell growth and colony formation in vitro. In a subcutaneous xenograft model, GSTO2‐transfected cells formed smaller tumors in nude mice than mock‐transfected cells. Upon intravenous injection into nude mice, the incidence of liver metastasis was lower in mice injected with GSTO2‐transfected cells than in those injected with mock‐transfected cells. In addition, GSTO2 induction suppressed the expression of β‐catenin and the oxygen consumption rate, but it did not affect the extracellular acidification rate. Furthermore, GSTO2‐transfected cells displayed lower mitochondrial membrane potential than mock‐transfected cells. When GSTO2‐transfected cells were treated with a p38 inhibitor, β‐catenin expression and mitochondrial membrane potential were recovered. Our study indicated that the loss of GSTO2 via DNA hypermethylation contributes to the growth and progression of LSCC, probably by modulating cancer metabolism via the p38/β‐catenin signaling pathway. Glutathione S‐transferase omega 2 (GSTO2) is expressed in the stem cells of the bronchial and alveolar epithelium. Loss of GSTO2 might contribute to lung squamous cell carcinoma growth by modulating cancer metabolism via the p38/β‐catenin signaling pathway. Glutathione S‐transferase omega 2 (GSTO2) lacks any appreciable GST activity, but it exhibits thioltransferase activity. The significance of GSTO2 in lung function has been reported; however, the precise expression and molecular function of GSTO2 in the lungs remain unclear. In the present study, we found that GSTO2 is expressed in airway basal cells, non–ciliated, columnar Clara cells, and type II alveolar cells, which have self‐renewal capacity in the lungs. Contrastingly, no GSTO2 expression was observed in 94 lung squamous cell carcinoma (LSCC) samples. When human LSCC cell lines were treated with 5‐aza‐2′‐deoxycytidine, a DNA‐methyltransferase inhibitor, GSTO2 transcription was induced, suggesting that aberrant GSTO2 hypermethylation in LSCC is the cause of its downregulation. Forced GSTO2 expression in LSCC cell lines inhibited cell growth and colony formation in vitro. In a subcutaneous xenograft model, GSTO2‐transfected cells formed smaller tumors in nude mice than mock‐transfected cells. Upon intravenous injection into nude mice, the incidence of liver metastasis was lower in mice injected with GSTO2‐transfected cells than in those injected with mock‐transfected cells. In addition, GSTO2 induction suppressed the expression of β‐catenin and the oxygen consumption rate, but it did not affect the extracellular acidification rate. Furthermore, GSTO2‐transfected cells displayed lower mitochondrial membrane potential than mock‐transfected cells. When GSTO2‐transfected cells were treated with a p38 inhibitor, β‐catenin expression and mitochondrial membrane potential were recovered. Our study indicated that the loss of GSTO2 via DNA hypermethylation contributes to the growth and progression of LSCC, probably by modulating cancer metabolism via the p38/β‐catenin signaling pathway. Glutathione S‐transferase omega 2 (GSTO2) is expressed in the stem cells of the bronchial and alveolar epithelium. Loss of GSTO2 might contribute to lung squamous cell carcinoma growth by modulating cancer metabolism via the p38/β‐catenin signaling pathway. Glutathione S-transferase omega 2 (GSTO2) lacks any appreciable GST activity, but it exhibits thioltransferase activity. The significance of GSTO2 in lung function has been reported; however, the precise expression and molecular function of GSTO2 in the lungs remain unclear. In the present study, we found that GSTO2 is expressed in airway basal cells, non-ciliated, columnar Clara cells, and type II alveolar cells, which have self-renewal capacity in the lungs. Contrastingly, no GSTO2 expression was observed in 94 lung squamous cell carcinoma (LSCC) samples. When human LSCC cell lines were treated with 5-aza-2'-deoxycytidine, a DNA-methyltransferase inhibitor, GSTO2 transcription was induced, suggesting that aberrant GSTO2 hypermethylation in LSCC is the cause of its downregulation. Forced GSTO2 expression in LSCC cell lines inhibited cell growth and colony formation in vitro. In a subcutaneous xenograft model, GSTO2-transfected cells formed smaller tumors in nude mice than mock-transfected cells. Upon intravenous injection into nude mice, the incidence of liver metastasis was lower in mice injected with GSTO2-transfected cells than in those injected with mock-transfected cells. In addition, GSTO2 induction suppressed the expression of β-catenin and the oxygen consumption rate, but it did not affect the extracellular acidification rate. Furthermore, GSTO2-transfected cells displayed lower mitochondrial membrane potential than mock-transfected cells. When GSTO2-transfected cells were treated with a p38 inhibitor, β-catenin expression and mitochondrial membrane potential were recovered. Our study indicated that the loss of GSTO2 via DNA hypermethylation contributes to the growth and progression of LSCC, probably by modulating cancer metabolism via the p38/β-catenin signaling pathway.Glutathione S-transferase omega 2 (GSTO2) lacks any appreciable GST activity, but it exhibits thioltransferase activity. The significance of GSTO2 in lung function has been reported; however, the precise expression and molecular function of GSTO2 in the lungs remain unclear. In the present study, we found that GSTO2 is expressed in airway basal cells, non-ciliated, columnar Clara cells, and type II alveolar cells, which have self-renewal capacity in the lungs. Contrastingly, no GSTO2 expression was observed in 94 lung squamous cell carcinoma (LSCC) samples. When human LSCC cell lines were treated with 5-aza-2'-deoxycytidine, a DNA-methyltransferase inhibitor, GSTO2 transcription was induced, suggesting that aberrant GSTO2 hypermethylation in LSCC is the cause of its downregulation. Forced GSTO2 expression in LSCC cell lines inhibited cell growth and colony formation in vitro. In a subcutaneous xenograft model, GSTO2-transfected cells formed smaller tumors in nude mice than mock-transfected cells. Upon intravenous injection into nude mice, the incidence of liver metastasis was lower in mice injected with GSTO2-transfected cells than in those injected with mock-transfected cells. In addition, GSTO2 induction suppressed the expression of β-catenin and the oxygen consumption rate, but it did not affect the extracellular acidification rate. Furthermore, GSTO2-transfected cells displayed lower mitochondrial membrane potential than mock-transfected cells. When GSTO2-transfected cells were treated with a p38 inhibitor, β-catenin expression and mitochondrial membrane potential were recovered. Our study indicated that the loss of GSTO2 via DNA hypermethylation contributes to the growth and progression of LSCC, probably by modulating cancer metabolism via the p38/β-catenin signaling pathway. |
| Author | Terayama, Masayoshi Sekihara, Keigo Hagiwara, Teruki Kawamura, Yuki I. Miyazaki, Hideki Igari, Toru Sumiya, Ryusuke Nagasaka, Satoshi Nakata, Kazuaki Yamada, Kazuhiko |
| AuthorAffiliation | 4 Department of Surgery National Center for Global Health and Medicine Tokyo Japan 1 Department of Gastroenterology The Research Center for Hepatitis and Immunology, Research Institute National Center for Global Health and Medicine Chiba Japan 2 Department of Thoracic Surgery National Center for Global Health and Medicine Tokyo Japan 5 Pathology Division of Clinical Laboratory National Center for Global Health and Medicine Tokyo Japan 3 Course of Advanced and Specialized Medicine Juntendo University Graduate School of Medicine Tokyo Japan 6 Present address: Department of Gastroenterological Surgery Gastroenterological Center Cancer Institute Hospital Japanese Foundation for Cancer Research Tokyo Japan |
| AuthorAffiliation_xml | – name: 2 Department of Thoracic Surgery National Center for Global Health and Medicine Tokyo Japan – name: 3 Course of Advanced and Specialized Medicine Juntendo University Graduate School of Medicine Tokyo Japan – name: 6 Present address: Department of Gastroenterological Surgery Gastroenterological Center Cancer Institute Hospital Japanese Foundation for Cancer Research Tokyo Japan – name: 5 Pathology Division of Clinical Laboratory National Center for Global Health and Medicine Tokyo Japan – name: 1 Department of Gastroenterology The Research Center for Hepatitis and Immunology, Research Institute National Center for Global Health and Medicine Chiba Japan – name: 4 Department of Surgery National Center for Global Health and Medicine Tokyo Japan |
| Author_xml | – sequence: 1 givenname: Ryusuke orcidid: 0000-0002-2464-6717 surname: Sumiya fullname: Sumiya, Ryusuke organization: Juntendo University Graduate School of Medicine – sequence: 2 givenname: Masayoshi surname: Terayama fullname: Terayama, Masayoshi organization: National Center for Global Health and Medicine – sequence: 3 givenname: Teruki surname: Hagiwara fullname: Hagiwara, Teruki organization: National Center for Global Health and Medicine – sequence: 4 givenname: Kazuaki surname: Nakata fullname: Nakata, Kazuaki organization: National Center for Global Health and Medicine – sequence: 5 givenname: Keigo surname: Sekihara fullname: Sekihara, Keigo organization: National Center for Global Health and Medicine – sequence: 6 givenname: Satoshi surname: Nagasaka fullname: Nagasaka, Satoshi organization: National Center for Global Health and Medicine – sequence: 7 givenname: Hideki surname: Miyazaki fullname: Miyazaki, Hideki organization: National Center for Global Health and Medicine – sequence: 8 givenname: Toru surname: Igari fullname: Igari, Toru organization: National Center for Global Health and Medicine – sequence: 9 givenname: Kazuhiko surname: Yamada fullname: Yamada, Kazuhiko organization: National Center for Global Health and Medicine – sequence: 10 givenname: Yuki I. surname: Kawamura fullname: Kawamura, Yuki I. email: kawamura@hospk.ncgm.go.jp organization: National Center for Global Health and Medicine |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/34726807$$D View this record in MEDLINE/PubMed |
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| CitedBy_id | crossref_primary_10_3390_ijms25189961 crossref_primary_10_1002_rmb2_12504 crossref_primary_10_3389_fmolb_2025_1506961 crossref_primary_10_1007_s10555_022_10077_9 crossref_primary_10_1007_s13167_024_00357_5 crossref_primary_10_3389_fphar_2024_1360352 |
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| Copyright | 2021 The Authors. published by John Wiley & Sons Australia, Ltd on behalf of Japanese Cancer Association. 2021 The Authors. Cancer Science published by John Wiley & Sons Australia, Ltd on behalf of Japanese Cancer Association. 2022. 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 | Glutathione S‐transferase omega 2 (GSTO2) lacks any appreciable GST activity, but it exhibits thioltransferase activity. The significance of GSTO2 in lung... Glutathione S-transferase omega 2 (GSTO2) lacks any appreciable GST activity, but it exhibits thioltransferase activity. The significance of GSTO2 in lung... |
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| SubjectTerms | Acidification Alveoli Animals Basal cells cancer metabolism Carcinoma, Squamous Cell - genetics Carcinoma, Squamous Cell - pathology Catenin Cell growth Cell Line, Tumor Chronic obstructive pulmonary disease Decitabine - pharmacology Deoxyribonucleic acid DNA DNA Methylation - drug effects DNA methyltransferase Down-Regulation - drug effects Epigenesis, Genetic Gene expression Gene Expression Regulation, Neoplastic - drug effects Glutathione Glutathione Transferase - genetics Glycolysis GSTO2 Humans Intravenous administration Kinases Laboratories Liver Neoplasms - genetics Liver Neoplasms - pathology Liver Neoplasms - secondary LSCC Lung cancer Lung carcinoma Lung Neoplasms - genetics Lung Neoplasms - pathology Male MAP Kinase Signaling System - drug effects Membrane potential Metabolism Metastases Mice Mice, Nude Mitochondria Mutation Neoplasm Transplantation Original Oxidative Phosphorylation Oxygen consumption p38 Respiratory function Signal transduction Squamous cell carcinoma Stem cells Transcription Xenografts β‐catenin |
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| Title | Loss of GSTO2 contributes to cell growth and mitochondria function via the p38 signaling in lung squamous cell carcinoma |
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