Atorvastatin inhibits glioma glycolysis and immune escape by modulating the miR-125a-5p/TXLNA axis
Abstract Background Conventional treatments, including surgery, radiotherapy and chemotherapy, have many limitations in the prognosis of glioma patients. Atorvastatin (ATOR) has a significant inhibitory effect on glioma malignancy. Thus, ATOR may play a key role in the search for new drugs for the e...
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BMC
2024-12-01
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| Series: | Hereditas |
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| Online Access: | https://doi.org/10.1186/s41065-024-00349-5 |
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| author | Kang Gao Tao Zhou YingChun Yin XiaoJie Sun HePing Jiang TangYue Li |
| author_facet | Kang Gao Tao Zhou YingChun Yin XiaoJie Sun HePing Jiang TangYue Li |
| author_sort | Kang Gao |
| collection | DOAJ |
| description | Abstract Background Conventional treatments, including surgery, radiotherapy and chemotherapy, have many limitations in the prognosis of glioma patients. Atorvastatin (ATOR) has a significant inhibitory effect on glioma malignancy. Thus, ATOR may play a key role in the search for new drugs for the effective treatment of gliomas. Methods U87 cells were treated with different doses of ATOR and transfected. Viability was assessed using MTT, proliferative ability was determined using the colony formation test, Bax and Bcl-2 were identified using Western blot, apoptosis was identified using flow cytometry, and U87 cell migration and invasion were detected using the Transwell assay. Glucose uptake, lactate secretion, and ATP production in U87 cell culture medium were quantified. The positive rates of IFN-γ and TNF-α in CD8T were measured through flow cytometry. Subcutaneous injection of U87 cells was carried out to construct an in vivo mouse model of gliom, followed by HE staining to assess the effects of ATOR and miR-125a-5p on tumor development. Results ATOR blocked the viability, proliferation, migration, and invasion of U87 cells through the miR-125a-5p/TXLNA axis, and suppressed glycolysis and immune escape of glioma cells. Furthermore, overexpressing miR-125a-5p enhanced the anti-tumor effect of ATOR in vivo. Conclusion ATOR blocks glioma progression by modulating the miR-125a-5p/TXLNA axis, further demonstrating that ATOR provides an effective therapeutic target for the treatment of glioma. |
| format | Article |
| id | doaj-art-788e4411e08f4002b0ff1e1c4d442e7f |
| institution | Kabale University |
| issn | 1601-5223 |
| language | English |
| publishDate | 2024-12-01 |
| publisher | BMC |
| record_format | Article |
| series | Hereditas |
| spelling | doaj-art-788e4411e08f4002b0ff1e1c4d442e7f2024-12-29T12:34:10ZengBMCHereditas1601-52232024-12-01161111410.1186/s41065-024-00349-5Atorvastatin inhibits glioma glycolysis and immune escape by modulating the miR-125a-5p/TXLNA axisKang Gao0Tao Zhou1YingChun Yin2XiaoJie Sun3HePing Jiang4TangYue Li5Department of Neurosurgery, Central Hospital of ZiboDepartment of Neurosurgery, Central Hospital of ZiboDepartment of Pathology, Central Hospital of ZiboDepartment of Pathology, Central Hospital of ZiboDepartment of Neurosurgery, Central Hospital of ZiboDepartment of Pathology, Central Hospital of ZiboAbstract Background Conventional treatments, including surgery, radiotherapy and chemotherapy, have many limitations in the prognosis of glioma patients. Atorvastatin (ATOR) has a significant inhibitory effect on glioma malignancy. Thus, ATOR may play a key role in the search for new drugs for the effective treatment of gliomas. Methods U87 cells were treated with different doses of ATOR and transfected. Viability was assessed using MTT, proliferative ability was determined using the colony formation test, Bax and Bcl-2 were identified using Western blot, apoptosis was identified using flow cytometry, and U87 cell migration and invasion were detected using the Transwell assay. Glucose uptake, lactate secretion, and ATP production in U87 cell culture medium were quantified. The positive rates of IFN-γ and TNF-α in CD8T were measured through flow cytometry. Subcutaneous injection of U87 cells was carried out to construct an in vivo mouse model of gliom, followed by HE staining to assess the effects of ATOR and miR-125a-5p on tumor development. Results ATOR blocked the viability, proliferation, migration, and invasion of U87 cells through the miR-125a-5p/TXLNA axis, and suppressed glycolysis and immune escape of glioma cells. Furthermore, overexpressing miR-125a-5p enhanced the anti-tumor effect of ATOR in vivo. Conclusion ATOR blocks glioma progression by modulating the miR-125a-5p/TXLNA axis, further demonstrating that ATOR provides an effective therapeutic target for the treatment of glioma.https://doi.org/10.1186/s41065-024-00349-5GliomaAtorvastatinmiR-125a-5pTXLNAGlycolysisImmune escape |
| spellingShingle | Kang Gao Tao Zhou YingChun Yin XiaoJie Sun HePing Jiang TangYue Li Atorvastatin inhibits glioma glycolysis and immune escape by modulating the miR-125a-5p/TXLNA axis Hereditas Glioma Atorvastatin miR-125a-5p TXLNA Glycolysis Immune escape |
| title | Atorvastatin inhibits glioma glycolysis and immune escape by modulating the miR-125a-5p/TXLNA axis |
| title_full | Atorvastatin inhibits glioma glycolysis and immune escape by modulating the miR-125a-5p/TXLNA axis |
| title_fullStr | Atorvastatin inhibits glioma glycolysis and immune escape by modulating the miR-125a-5p/TXLNA axis |
| title_full_unstemmed | Atorvastatin inhibits glioma glycolysis and immune escape by modulating the miR-125a-5p/TXLNA axis |
| title_short | Atorvastatin inhibits glioma glycolysis and immune escape by modulating the miR-125a-5p/TXLNA axis |
| title_sort | atorvastatin inhibits glioma glycolysis and immune escape by modulating the mir 125a 5p txlna axis |
| topic | Glioma Atorvastatin miR-125a-5p TXLNA Glycolysis Immune escape |
| url | https://doi.org/10.1186/s41065-024-00349-5 |
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