Telmisartan attenuates human glioblastoma cells proliferation and oncogenicity by inducing the lipid oxidation
Autor: | Baohui Xu, Chen Li, Jia Guo, Tengrui Zhang, Yan Wang, Lixiang Xue |
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Rok vydání: | 2021 |
Předmět: |
Oncogenicity
Benzoates 03 medical and health sciences 0302 clinical medicine Western blot Lipid oxidation medicine Humans Telmisartan 030212 general & internal medicine Receptor Cell Proliferation medicine.diagnostic_test business.industry Lipid metabolism General Medicine Cell cycle Lipid Metabolism Lipids PPAR gamma Oncology Cell culture 030220 oncology & carcinogenesis Cancer research Benzimidazoles Glioblastoma business medicine.drug |
Zdroj: | Asia-Pacific Journal of Clinical Oncology. 18:217-223 |
ISSN: | 1743-7563 1743-7555 |
DOI: | 10.1111/ajco.13574 |
Popis: | BACKGROUND Glioblastoma (GBM) is one of the most common primary brain tumors, which accounts up to 80% of malignant brain tumors and the 5-year relative survival rate is below 5%. Recent studies showed that the lipid metabolism played an essential role in GBM development. As a peroxisome proliferators-activated receptors γ (PPAR-γ) agonist, telmisartan improves the lipid metabolism and has been used to treat hypertension for long time. It has also been shown to have anticancer function, such as in lung cancer and melanoma. METHODS Incucyte real-time live cell imaging system was used to assess the effect of telmisartan on glioma cell lines U87 and U251 proliferation. Transwell assay and colony formation assay were conducted to detect the effect of telmisartan on oncogenicity of GBM cell lines. Western blot and immunofluorescence analysis were used to detect the effect of telmisartan on the expression of PPAR-γ and hydroxyacyl-coenzyme A dehydrogenase alpha subunit (HADHA). RESULTS We demonstrate that telmisartan inhibits two glioma cell lines U87 and U251 proliferation in a time- and dose-dependent manner, and arrests the cell cycle at S phase. We further show that telmisartan decreases the oncogenicity of GBM cell lines. Our data show that telmisartan treatment significantly increases the PPAR-γ expression level, enhances the lipid oxidation, and upregulates the level of fatty acid oxidation key enzyme HADHA. CONCLUSIONS Telmisartan inhibits the proliferation and oncogenicity while it also increases the lipid oxidation of human GBM cells. |
Databáze: | OpenAIRE |
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