Genetic evidence that antioxidants can help treat cancer
Scientists have provided genetic evidence suggesting the antioxidant drugs currently used to treat lung disease, malaria and even the common cold can also help prevent and treat cancers because they fight against mitochondrial oxidative stress-a culprit in driving tumor growth.
For the first time, researchers from Jefferson's Kimmel Cancer Center show that loss of the tumor suppressor protein Caveolin-1 (Cav-1) induces mitochondrial oxidative stress in the stromal micro-environment, a process that fuels cancer cells in most common types of breast cancer.
"Now we have genetic proof that mitochondrial oxidative stress is important for driving tumor growth," said lead researcher Michael P. Lisanti.
"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," he said.
In the study, Jefferson researchers applied a genetically tractable model for human cancer associated fibroblasts using a targeted sh-RNA knock-down approach.
Without the Cav-1 protein, researchers found that oxidative stress in cancer associated fibroblasts leads to mitochondrial dysfunction in stromal fibroblasts.
In this context, oxidative stress and the resulting autophagy (producton of recycled nutrients) in the tumor-microenvironment function as metabolic energy or "food" to "fuel" tumor growth.
The researchers report that the loss of Cav-1 increases mitochondrial oxidative stress in the tumor stroma, increasing both tumor mass and tumor volume by four-fold, without any increase in tumor angiogenesis.
"This study provides the necessary genetic evidence that reducing oxidative stress in the body will decrease tumor growth," Lisanti said
These findings were published in the online February 15 issue of Cancer Biology and Therapy.
For the first time, researchers from Jefferson's Kimmel Cancer Center show that loss of the tumor suppressor protein Caveolin-1 (Cav-1) induces mitochondrial oxidative stress in the stromal micro-environment, a process that fuels cancer cells in most common types of breast cancer.
"Now we have genetic proof that mitochondrial oxidative stress is important for driving tumor growth," said lead researcher Michael P. Lisanti.
"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," he said.
In the study, Jefferson researchers applied a genetically tractable model for human cancer associated fibroblasts using a targeted sh-RNA knock-down approach.
Without the Cav-1 protein, researchers found that oxidative stress in cancer associated fibroblasts leads to mitochondrial dysfunction in stromal fibroblasts.
In this context, oxidative stress and the resulting autophagy (producton of recycled nutrients) in the tumor-microenvironment function as metabolic energy or "food" to "fuel" tumor growth.
The researchers report that the loss of Cav-1 increases mitochondrial oxidative stress in the tumor stroma, increasing both tumor mass and tumor volume by four-fold, without any increase in tumor angiogenesis.
"This study provides the necessary genetic evidence that reducing oxidative stress in the body will decrease tumor growth," Lisanti said
These findings were published in the online February 15 issue of Cancer Biology and Therapy.
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