ST1926 inhibits glioma progression through regulating mitochondrial complex II - 18/06/20
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Highlights |
• | ST1926 suppresses cell viability, reduces ATP production and induces AMPKα activation in glioma cells. |
• | ST1926 results in mitochondrial dysfunction in glioma cells. |
• | ST1926 significantly induced apoptosis associated with ROS accumulation in glioma cells. |
• | ST1926 reduces glioma cells mitochondrial CII activity and suppresses tumor growth. |
Abstract |
The antitumor activity of atypical adamantyl retinoid ST1926 has been frequently reported in cancer studies; nevertheless, its effect on glioma has not been fully understood. Mitochondria are critical in regulating tumorigenesis and are defined as a promising target for anti-tumor therapy. In the present study, we found that ST1926 might be a mitochondria-targeting anti-glioma drug. ST1926 showed significantly inhibitory role in the viability of glioma cells mainly through inducing apoptosis and autophagy. The results showed that ST1926 alleviated mitochondria-regulated bioenergetics in glioma cells via reducing ATP production and promoting reactive oxygen species production. Importantly, ST1926 significantly impaired complex II (CII) function, which was associated with the inhibition of succinate dehydrogenase (SDH) activity. In addition, the effects of ST1926 on the induction of apoptosis and ROS were further promoted by the treatment of CII inhibitors, including TTFA and 3-NPA. Furthermore, the in vivo experiments confirmed the role of ST1926 in suppressing xenograft tumor growth with few toxicity. Therefore, ST1926 might be an effective anti-glioma drug through targeting CII.
El texto completo de este artículo está disponible en PDF.Keywords : ST1926, Glioma, Apoptosis, Mitochondria, Complex II
Esquema
Vol 128
Artículo 110291- août 2020 Regresar al númeroBienvenido a EM-consulte, la referencia de los profesionales de la salud.
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