The Effect of Liraglutide on Lung Cancer and Its Potential Protective Effect on High Glucose-Induced Lung Senescence and Oxidative Damage
Background: Lung cancer is a malignant disease with high morbidity and mortality. Lung cancer and diabetes are closely related, and diabetic patients with lung tumors are common in clinical practice. Liraglutide, a glucagon-like peptide-1 receptor (GLP-1R) agonist, is commonly used in the treatment...
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| Format: | Article |
| Language: | English |
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IMR Press
2023-10-01
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| Series: | Frontiers in Bioscience-Landmark |
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| Online Access: | https://www.imrpress.com/journal/FBL/28/10/10.31083/j.fbl2810259 |
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| author | Zhiyan Pu Yanxia Yang Shuanghong Qin Xiaojuan Li Can Cui Weiyu Chen |
| author_facet | Zhiyan Pu Yanxia Yang Shuanghong Qin Xiaojuan Li Can Cui Weiyu Chen |
| author_sort | Zhiyan Pu |
| collection | DOAJ |
| description | Background: Lung cancer is a malignant disease with high morbidity and mortality. Lung cancer and diabetes are closely related, and diabetic patients with lung tumors are common in clinical practice. Liraglutide, a glucagon-like peptide-1 receptor (GLP-1R) agonist, is commonly used in the treatment of type 2 diabetes. In this study, we examined the effect of liraglutide on lung cancer and its potential protective effect on high glucose-induced lung aging. Methods: Indirect mmunofluorescence was done to assess the expression levels of p-AKT, ki67, Caspase3, Bax and PI3K. Western blotting was conducted to determine the expression levels of BAX, BCL2, Caspase9, E-cadherin, N-cadherin, PI3K, AKT and vimentin. Cell viability, cell cycle and cell apoptosis were evaluated by colony formation, CCK-8 assay and flow cytometry. Immunohistochemistry was performed to evaluate the expression of Nf-κb, p15, p16, p21 and SMA in vivo. Besides, a high glucose-induced lung cell injury model was established to evaluate the effect of liraglutide on lung aging and oxidative damage. Sa-β-gal staining was used to assess cellular/ tissue senescence. Cell senescence-related markers (p16, p21 and p53 ) were determined by Western-blot analysis. Results: The proliferation, cell cycle, migration of lung cancer cells were significantly inhibited after treatment with liraglutide compared to control group (p < 0.05). Furthermore, Liraglutide inhibited the epithelial–mesenchymal transition process of lung cancer cell compared to control group (p < 0.05). Liraglutide also suppressed the proliferation of lung cancer in vivo. Besides, the BEAS-2B cell senescence induced by high glucose was significantly alleviated after treatment with liraglutide compared with control group (p < 0.05). The lung aging and endoplasmic reticulum stress was significantly suppressed after liraglutide treatment. Conclusions: This work indicates that liraglutide could inhibit lung cancer cell proliferation in vitro and in vivo. In addition, liraglutide exhibited anti-aging effects in vivo and in vivo. The current work has important implications for the treatment of patients with diabetes and lung cancer. |
| first_indexed | 2024-03-11T13:29:55Z |
| format | Article |
| id | doaj.art-e25e5cebf9f04e518fcb71e827b02101 |
| institution | Directory Open Access Journal |
| issn | 2768-6701 |
| language | English |
| last_indexed | 2024-03-11T13:29:55Z |
| publishDate | 2023-10-01 |
| publisher | IMR Press |
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| series | Frontiers in Bioscience-Landmark |
| spelling | doaj.art-e25e5cebf9f04e518fcb71e827b021012023-11-03T02:31:25ZengIMR PressFrontiers in Bioscience-Landmark2768-67012023-10-01281025910.31083/j.fbl2810259S2768-6701(23)00864-XThe Effect of Liraglutide on Lung Cancer and Its Potential Protective Effect on High Glucose-Induced Lung Senescence and Oxidative DamageZhiyan Pu0Yanxia Yang1Shuanghong Qin2Xiaojuan Li3Can Cui4Weiyu Chen5Department of Endocrinology, The Second People's Hospital of Gansu Province, Northwest Minzu University, 730000 Lanzhou, Gansu, ChinaDepartment of Endocrinology, The Second People's Hospital of Gansu Province, Northwest Minzu University, 730000 Lanzhou, Gansu, ChinaDepartment of Endocrinology, The Second People's Hospital of Gansu Province, Northwest Minzu University, 730000 Lanzhou, Gansu, ChinaDepartment of Endocrinology, The Second People's Hospital of Gansu Province, Northwest Minzu University, 730000 Lanzhou, Gansu, ChinaDepartment of Endocrinology, Second Affiliated Hospital of Harbin Medical University, 150086 Harbin, Heilongjiang, ChinaDepartment of Endocrinology, The Second People's Hospital of Gansu Province, Northwest Minzu University, 730000 Lanzhou, Gansu, ChinaBackground: Lung cancer is a malignant disease with high morbidity and mortality. Lung cancer and diabetes are closely related, and diabetic patients with lung tumors are common in clinical practice. Liraglutide, a glucagon-like peptide-1 receptor (GLP-1R) agonist, is commonly used in the treatment of type 2 diabetes. In this study, we examined the effect of liraglutide on lung cancer and its potential protective effect on high glucose-induced lung aging. Methods: Indirect mmunofluorescence was done to assess the expression levels of p-AKT, ki67, Caspase3, Bax and PI3K. Western blotting was conducted to determine the expression levels of BAX, BCL2, Caspase9, E-cadherin, N-cadherin, PI3K, AKT and vimentin. Cell viability, cell cycle and cell apoptosis were evaluated by colony formation, CCK-8 assay and flow cytometry. Immunohistochemistry was performed to evaluate the expression of Nf-κb, p15, p16, p21 and SMA in vivo. Besides, a high glucose-induced lung cell injury model was established to evaluate the effect of liraglutide on lung aging and oxidative damage. Sa-β-gal staining was used to assess cellular/ tissue senescence. Cell senescence-related markers (p16, p21 and p53 ) were determined by Western-blot analysis. Results: The proliferation, cell cycle, migration of lung cancer cells were significantly inhibited after treatment with liraglutide compared to control group (p < 0.05). Furthermore, Liraglutide inhibited the epithelial–mesenchymal transition process of lung cancer cell compared to control group (p < 0.05). Liraglutide also suppressed the proliferation of lung cancer in vivo. Besides, the BEAS-2B cell senescence induced by high glucose was significantly alleviated after treatment with liraglutide compared with control group (p < 0.05). The lung aging and endoplasmic reticulum stress was significantly suppressed after liraglutide treatment. Conclusions: This work indicates that liraglutide could inhibit lung cancer cell proliferation in vitro and in vivo. In addition, liraglutide exhibited anti-aging effects in vivo and in vivo. The current work has important implications for the treatment of patients with diabetes and lung cancer.https://www.imrpress.com/journal/FBL/28/10/10.31083/j.fbl2810259liraglutidelung cancerproliferationaginglung cells |
| spellingShingle | Zhiyan Pu Yanxia Yang Shuanghong Qin Xiaojuan Li Can Cui Weiyu Chen The Effect of Liraglutide on Lung Cancer and Its Potential Protective Effect on High Glucose-Induced Lung Senescence and Oxidative Damage Frontiers in Bioscience-Landmark liraglutide lung cancer proliferation aging lung cells |
| title | The Effect of Liraglutide on Lung Cancer and Its Potential Protective Effect on High Glucose-Induced Lung Senescence and Oxidative Damage |
| title_full | The Effect of Liraglutide on Lung Cancer and Its Potential Protective Effect on High Glucose-Induced Lung Senescence and Oxidative Damage |
| title_fullStr | The Effect of Liraglutide on Lung Cancer and Its Potential Protective Effect on High Glucose-Induced Lung Senescence and Oxidative Damage |
| title_full_unstemmed | The Effect of Liraglutide on Lung Cancer and Its Potential Protective Effect on High Glucose-Induced Lung Senescence and Oxidative Damage |
| title_short | The Effect of Liraglutide on Lung Cancer and Its Potential Protective Effect on High Glucose-Induced Lung Senescence and Oxidative Damage |
| title_sort | effect of liraglutide on lung cancer and its potential protective effect on high glucose induced lung senescence and oxidative damage |
| topic | liraglutide lung cancer proliferation aging lung cells |
| url | https://www.imrpress.com/journal/FBL/28/10/10.31083/j.fbl2810259 |
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