Researchers from Jefferson’s Kimmel Cancer Center have evidence that dietary supplements can be used to treat cancer, lung disease, malaria and even the common cold.
They do so by fighting mitochondrial oxidative stress – a driving force for tumor growth. The research showed that loss of a tumor suppressor protein called Cavolin-1 (Cav-1) induces mitochondrial oxidative stress, a process that fuels cancer cells in most types of breast cancer.
Lead researcher, Michael Lisanti, M.D and his lab had previously discovered Cav-1 as a biomarker that functions as a tumor suppressor and is a predictor of patient outcome in breast cancer cases. The presence of Cav-1 protein indicates a greater chance of survival. They also confirmed Cav-1’s role in oxidative stress and tumor growth but didn’t know why the stress was occurring.
"Now we have genetic proof that mitochondrial oxidative stress is important for driving tumor growth," said Michael P. Lisanti, M.D, professor of cancer biology at Jefferson Medical College of Thomas Jefferson University. "This means we need to make anti-cancer drugs that specially target this type of oxidative stress. And there are already antioxidant drugs out there on the market as dietary supplements, like N-acetyl cysteine. We are not taking advantage of the available drugs that reduce oxidative stress and autophagy, including metformin, chloroquine and N-acetyl cysteine. Now that we have genetic proof that oxidative stress and resulting autophagy are important for driving tumor growth, we should re-consider using antioxidants and autophagy inhibitors as anti-cancer agents."
Antioxidants aren’t currently used as a conventional therapy for cancer because it was thought that they would interfere with chemotherapy (chemotherapy increases oxidative stress).
Without Cav-1, there was mitochondrial dysfunction, leading to oxidative stress and autophagy (production of recycled nutrients) as metabolic energy or "food" to feed tumor growth.
"Antioxidants have been associated with cancer reducing effects—beta carotene, for example—but the mechanisms, the genetic evidence, has been lacking," Lisanti said.