Scientists say a form of Vitamin E may be able to help fight malignant mesothelioma by limiting the growth of tumor-feeding blood vessels.
Researchers with Toyo University’s Graduate School of Life Sciences in Japan recently released a study on the redox-silent tocotrienol (Vitamin E) analog 6-O-carboxypropyl-α-tocotrienol – called T3E – and its impact on mesothelioma. Although previous studies have found T3E to have powerful anti-cancer properties, the goal of the new study was to better understand its mechanism in mesothelioma cells.
According to a report in Biological and Pharmaceutical Bulletin, T3E worked against mesothelioma cells by inhibiting the expression of vascular endothelial growth factor (VEGF), a signaling protein that supplies fresh oxygen to cells by stimulating the growth of new blood vessels. The news moves T3E a step closer to potential therapeutic use against mesothelioma, an aggressive cancer with no cure.
To stimulate VEGF production in mesothelioma cells, the research team first mimicked a low-oxygen environment with a chemical called cobalt chloride (CoCI2). When the mesothelioma cells responded to the low oxygen by increasing their production of VEGF, the cells were treated with T3E.
“T3E inhibited CoCI2-induced gene expression of VEGF due to the inactivation of Yes/HIF-2 α [gene] signaling,” lead author Ayami Sato writes in the newly-published report. “These data suggest that Yes/HIF-2 α/VEGF could be a promising therapeutic target of T3E in malignant mesothelioma cells.”
Unlike traditional chemotherapy drugs designed to poison cancer cells from the outside, T3E represents a new kind of cancer therapy that targets and kills cancer cells from the inside out by manipulating their genes. This approach is considered one of the most promising lines of research for patients with mesothelioma and other rare and intractable cancers.
Sato, A, et al, “A redox-silent analogue of tocotrienol inhibits cobalt(II) chloride-induced VEGF expression via Yes signaling in mesothelioma cells”, Biological and Pharmaceutical Bulletin. 2014, pp. 865-70