Research Paper Volume 9, Issue 10 pp 2098—2116
A new mutation-independent approach to cancer therapy: Inhibiting oncogenic RAS and MYC, by targeting mitochondrial biogenesis
Figure 11. MYC-RAS co-operativity “fuels” stemness in cancer cells: Mutation-independent cancer therapy, with Doxycycline. Here, we show that either a i) genetic stimulus [oncogene activation (c-Myc or H-Ras (G12V)] or an ii) environmental stimulus [mitochondrial oxidative stress (chemically induced by Rotenone)] are both sufficient to drive metabolic reprogramming and increased CSC propagation. Nevertheless, the positive growth effects of these oncogenic stimuli can both be blocked using a mutation-independent or “phenotypic approach”, by employing Doxycycline.