Telmisartan attenuates human glioblastoma cells proliferation and oncogenicity by inducing the lipid oxidation

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.

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).

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.

Telmisartan inhibits the proliferation and oncogenicity while it also increases the lipid oxidation of human GBM cells.