TMEM164 promotes ferroptosis by selectively mediating ATG5-dependent autophagosome formation to inhibit the progression of LUAD
The study focuses on lung adenocarcinoma (LUAD), a predominant type of lung cancer. Despite advancements in diagnostics and molecular therapies, treatment remains challenging due to its low five-year survival rate. This study aims to investigate the role of the transmembrane protein TMEM164 in ferro...
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| Format: | Article |
| Language: | English |
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Taylor & Francis Group
2024-12-01
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| Series: | Autoimmunity |
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| Online Access: | https://www.tandfonline.com/doi/10.1080/08916934.2024.2410192 |
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| _version_ | 1850107778997157888 |
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| author | Yongxiang Su Lintao Li Junhai Chen Chao Gao |
| author_facet | Yongxiang Su Lintao Li Junhai Chen Chao Gao |
| author_sort | Yongxiang Su |
| collection | DOAJ |
| description | The study focuses on lung adenocarcinoma (LUAD), a predominant type of lung cancer. Despite advancements in diagnostics and molecular therapies, treatment remains challenging due to its low five-year survival rate. This study aims to investigate the role of the transmembrane protein TMEM164 in ferroptosis and anti-tumor immunity in LUAD, and to evaluate its potential as a therapeutic target. Through cellular experiments (such as QPCR, WB, CCK-8, EdU, Transwell, flow cytometry, CO-IP) and animal model experiments (including HE staining and IHC analysis), the relationship between TMEM164 expression and LUAD progression was explored, with particular attention to its mechanisms in ferroptosis and autophagy. The results show that TMEM164 expression is downregulated in LUAD and is associated with poor prognosis. Increasing TMEM164 expression significantly inhibits cell proliferation, migration, and invasion, while promoting an autophagy process dependent on ATG5 for autophagosome formation, thus facilitating ferroptosis. In mouse models, high TMEM164 expression combined with anti-PD-1 antibodies demonstrated synergistic anti-tumor effects. These findings highlight the critical role of TMEM164 in LUAD, suggesting that modulating TMEM164 expression could open new avenues for LUAD treatment. |
| format | Article |
| id | doaj-art-a9c187a12dd145a0a6fd05f8edbc15cb |
| institution | OA Journals |
| issn | 0891-6934 1607-842X |
| language | English |
| publishDate | 2024-12-01 |
| publisher | Taylor & Francis Group |
| record_format | Article |
| series | Autoimmunity |
| spelling | doaj-art-a9c187a12dd145a0a6fd05f8edbc15cb2025-08-20T02:38:31ZengTaylor & Francis GroupAutoimmunity0891-69341607-842X2024-12-0157110.1080/08916934.2024.2410192TMEM164 promotes ferroptosis by selectively mediating ATG5-dependent autophagosome formation to inhibit the progression of LUADYongxiang Su0Lintao Li1Junhai Chen2Chao Gao3Department of Surgical oncology, Fudan University Shanghai Cancer Center Xiamen Hospital (Xiamen Cancer Hospital), Xiamen City, ChinaDepartment of Thoracic Surgery, The First Affiliated Hospital of Xiamen University, Xiamen City, ChinaDepartment of Thoracic Surgery, The First Affiliated Hospital of Xiamen University, Xiamen City, ChinaDepartment of Surgical oncology, Fudan University Shanghai Cancer Center Xiamen Hospital (Xiamen Cancer Hospital), Xiamen City, ChinaThe study focuses on lung adenocarcinoma (LUAD), a predominant type of lung cancer. Despite advancements in diagnostics and molecular therapies, treatment remains challenging due to its low five-year survival rate. This study aims to investigate the role of the transmembrane protein TMEM164 in ferroptosis and anti-tumor immunity in LUAD, and to evaluate its potential as a therapeutic target. Through cellular experiments (such as QPCR, WB, CCK-8, EdU, Transwell, flow cytometry, CO-IP) and animal model experiments (including HE staining and IHC analysis), the relationship between TMEM164 expression and LUAD progression was explored, with particular attention to its mechanisms in ferroptosis and autophagy. The results show that TMEM164 expression is downregulated in LUAD and is associated with poor prognosis. Increasing TMEM164 expression significantly inhibits cell proliferation, migration, and invasion, while promoting an autophagy process dependent on ATG5 for autophagosome formation, thus facilitating ferroptosis. In mouse models, high TMEM164 expression combined with anti-PD-1 antibodies demonstrated synergistic anti-tumor effects. These findings highlight the critical role of TMEM164 in LUAD, suggesting that modulating TMEM164 expression could open new avenues for LUAD treatment.https://www.tandfonline.com/doi/10.1080/08916934.2024.2410192TMEM164ferroptosisautophagytumor immunityPD-1 |
| spellingShingle | Yongxiang Su Lintao Li Junhai Chen Chao Gao TMEM164 promotes ferroptosis by selectively mediating ATG5-dependent autophagosome formation to inhibit the progression of LUAD Autoimmunity TMEM164 ferroptosis autophagy tumor immunity PD-1 |
| title | TMEM164 promotes ferroptosis by selectively mediating ATG5-dependent autophagosome formation to inhibit the progression of LUAD |
| title_full | TMEM164 promotes ferroptosis by selectively mediating ATG5-dependent autophagosome formation to inhibit the progression of LUAD |
| title_fullStr | TMEM164 promotes ferroptosis by selectively mediating ATG5-dependent autophagosome formation to inhibit the progression of LUAD |
| title_full_unstemmed | TMEM164 promotes ferroptosis by selectively mediating ATG5-dependent autophagosome formation to inhibit the progression of LUAD |
| title_short | TMEM164 promotes ferroptosis by selectively mediating ATG5-dependent autophagosome formation to inhibit the progression of LUAD |
| title_sort | tmem164 promotes ferroptosis by selectively mediating atg5 dependent autophagosome formation to inhibit the progression of luad |
| topic | TMEM164 ferroptosis autophagy tumor immunity PD-1 |
| url | https://www.tandfonline.com/doi/10.1080/08916934.2024.2410192 |
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