Antioxidants Linked to Growth and Spread of Cancer Tumors, Study Finds
A recent study conducted by researchers at Karolinska Institutet in Sweden has revealed a surprising connection between antioxidants and the growth of cancer tumors. Antioxidants, including vitamins C and E, were found to activate a mechanism that stimulates the formation of new blood vessels in tumors, ultimately aiding their growth and spread.
In order to flourish and metastasize, cancer tumors require a constant supply of oxygen and nutrient-rich blood. This necessitates the development of new blood vessels, a process known as angiogenesis. When a tissue is deprived of oxygen, cancer cells in the affected area release chemical signals that prompt endothelial cells to create these new blood vessels.
The research team delved into the intricacies of angiogenesis and were astounded to discover the role that antioxidants play in tumor growth and spread. “We found that antioxidants activate a mechanism that leads to the formation of new blood vessels in cancer tumors, which is surprising because antioxidants were previously thought to be protective,” said Martin Bergö, the corresponding author of the study. The newly formed blood vessels provide nourishment to the tumor, facilitating its growth and spread.
Antioxidants are known for scavenging oxygen free radicals in the body’s cells, preventing or reducing damage caused by oxidative stress. Oxidative stress is associated with DNA damage and the development of various types of cancers, such as breast, lung, liver, colon, prostate, ovarian, and brain cancers.
While antioxidants found in common foods should not be feared, Berger advises against excessive consumption in most individuals. In fact, it could prove detrimental to cancer patients and those at high risk of developing cancer.
Prior studies have already shown that antioxidants, including vitamins C and E, accelerate the growth and spread of lung cancer by stabilizing a protein called BACH1. This protein is activated when the levels of free oxygen radicals in the body decrease, which occurs when additional antioxidants are consumed in the diet or when tumors develop spontaneous mutations that stimulate antioxidant production.
The research team primarily conducted lung cancer studies using lung cancer organoids grown from patients. However, they also examined mice and human breast and kidney tumor samples. They found that tumors that activated BACH1 through antioxidant intake or through overexpression of the BACH1 gene produced more new blood vessels and exhibited high sensitivity to angiogenesis inhibitors.
Angiogenesis inhibitors are drugs used to treat cancer, but their efficacy varies, and they often bring forth undesirable side effects. “Many clinical trials have evaluated the effectiveness of angiogenesis inhibitors, but the results were not as successful as expected,” stated Ting Wang, the first author of the study.
Additionally, the researchers discovered that BACH1 induces angiogenesis through a mechanism that does not require hypoxia, meaning tumors can form new blood vessels even in the presence of normal oxygen levels. BACH1 was also found to be regulated similarly to the protein hypoxia-inducible factor 1-alpha (HIF-1-alpha), which is associated with angiogenesis-driven tumor growth and metastasis. This suggests that the two proteins work together in tandem.
The implications of these findings are substantial. “Our study opens the door to more effective prevention of tumor angiogenesis,” declared Wang. Patients with higher levels of BACH1 in their tumors may benefit more from anti-angiogenic therapy than those with lower levels of BACH1.
The researchers are already looking ahead to future investigations. Their next step involves a thorough examination of how oxygen levels and free radicals regulate the BACH1 protein. They also plan to explore the clinical implications of these findings and expand their research to other cancers, including breast, kidney, and skin cancer.
The study, which was published in The Journal of Clinical Investigation, sheds new light on the role of antioxidants in cancer development and emphasizes the potential risks associated with unnecessary antioxidant supplementation.
In order to grow and metastasize, cancer tumors need a constant supply of oxygen and nutrient-rich blood. This requires the formation of new blood vessels on top of existing ones, a process known as angiogenesis. When tissue is starved of oxygen, cancer cells in the affected area send chemical signals that encourage endothelial cells to form new blood vessels.
Researchers at Karolinska Institutet in Sweden studied the mechanisms of angiogenesis and found that antioxidants play an unexpected role in the growth and spread of tumors.
Vitamin E (pixabay)
“We found that antioxidants activate a mechanism that leads to the formation of new blood vessels in cancer tumors, which is surprising because antioxidants were previously thought to be protective,” said Martin Bergö, corresponding author of the study. The new blood vessels nourish the tumor and help it grow and spread.”
Antioxidants typically scavenge oxygen free radicals in the body’s cells, preventing or reducing damage caused by oxidative stress. Oxidative stress is known to damage DNA and regulate the development of various cancers, including breast, lung, liver, colon, prostate, ovarian and brain cancers.
“Antioxidants in common foods should not be feared, but most people do not need to eat more of them,” says Berger. “In fact, it can be harmful to cancer patients and those at high risk of cancer.”
Researchers have previously shown that antioxidants such as vitamins C and E accelerate the growth and spread of lung cancer by stabilizing a protein called BACH1. The protein is activated when the levels of free oxygen radicals in the body decrease, which is the case when additional antioxidants are consumed in the diet, or when tumors develop spontaneous mutations that stimulate production antioxidants.
In the current study, the researchers conducted most of the lung cancer studies using lung cancer organoids grown from patients, but also studied mice and human breast and kidney tumor samples. Tumors that activated BACH1 through antioxidant intake or BACH1 gene overexpression were found to produce more new blood vessels and were highly sensitive to angiogenesis inhibitors.
BACH1 (public domain)
Drugs that inhibit angiogenesis are used to treat cancer with varying efficacy and nasty side effects.
“Many clinical trials have evaluated the effectiveness of angiogenesis inhibitors, but the results were not as successful as expected,” said Ting Wang, first author of the study.
The researchers found that BACH1 also induces angiogenesis through a mechanism that does not require hypoxia; that is, tumors can form new blood vessels in the presence of normal oxygen levels. BACH1 was also found to be similarly regulated by the protein hypoxia-inducible factor 1-alpha (HIF-1-alpha), whose expression is associated with angiogenesis-driven tumor growth and metastasis, suggesting that the two proteins work together.
“Our study opens the door to more effective prevention of tumor angiogenesis,” said Wang. “For example, patients with higher levels of BACH1 in their tumors may benefit more from anti-angiogenic therapy than patients with lower levels of BACH1.”
The researchers have already begun to look forward to future research, and the next step will be to examine in detail how oxygen levels and free radicals regulate the BACH1 protein, and they will continue to determine the clinical implications of the findings and their expansion in other cancers. , including breast cancer, kidney cancer and similar research skin cancer.
The study was published in The Journal of Clinical Investigation.
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