08/13/2018 / By Michelle Simmons
Researchers from Helmholtz Zentrum München, Technische Universität München (TUM), and Heidelberg University Hospital carried out a study on how extra weight makes breast cancer cells more aggressive. Using human tissue from breast cancer metastases, the researchers found that the enzyme known as ACC1 (acetyl-CoA-carboxylase 1) — a key component of fatty acid synthesis — is inhibited by high levels of cytokines. They found that obesity causes the release of cytokines into the bloodstream that affect the metabolism of breast cancer cells, which in turn make them more aggressive.
“ACC1 is a key component of fatty acid synthesis,” said Mauricio Berrel Diaz of Helmholtz Zentrum München and one of the leaders of the study. “However, its function is impaired by the cytokines leptin and TGF-?.”
Extremely overweight subjects have been found to have increased levels of cytokines in the blood. The researchers discovered that when ACC1 is inhibited, it results to the accumulation of the fatty acid precursor acetyl-CoA, which is passed on to particular gene “switches” that in turn stimulate the metastatic capacity of cancer cells through switching on a certain gene program.
In an experimental model, the researchers blocked the yet unknown signaling pathway with an antibody that is directed against the leptin receptor. This resulted to a significantly lowered metastatic spread of breast cancer cells. (Related: Breast Cancer Linked to Obesity in Women of All Ages, Leptin Probable Culprit.)
The researchers aim to prove the data on the recently discovered mechanism in future studies. Moreover, they are taking into consideration the related intervention points that could potentially be used for treating breast cancer.
“Blocking the signaling pathways and switching off the metastasis-related genes could be a therapeutic target,” explained Stephan Herzig of TUM and co-leader of the study. “As part of the so-called neoadjuvant therapy, the risk of metastases or the recurrence of tumors could be reduced prior to the surgical removal of the tumor.”
The findings of the study was published in the journal Cell Metabolism.
Being overweight or obese can result to health consequences. According to the Centers for Disease Control and Prevention (CDC), more than one-third or 36.5 percent of adults in the U.S. are obese. This makes them more vulnerable to serious health conditions, such as diabetes, cardiovascular disease, and some types of cancer. Women who became overweight or obese after menopause are more prone to having breast cancer.
According to an article by the American Cancer Society, before menopause, the ovaries produce most of the estrogen in the body, while fat tissue only produces a small amount. But after menopause, the ovaries stop producing estrogen, so most of a woman’s estrogen comes from fat tissue. Therefore, having more fat tissue after menopause can increase estrogen levels and raise the risk of developing breast cancer. Furthermore, women who are overweight or obese are more likely to have higher blood sugar levels, which have been associated to some types of cancer such as breast cancer.
Although this link is complicated, studies indicate that the increased risk seems to be on women who gained weight during their adulthood and not on those who have been overweight since childhood. In addition, having excess fat around the waist may increase the risk more compared to having excess fat in the hips and thighs.
In another entry by the American Cancer Society, it was written that breast cancer is the most common type of cancer in American women, except for skin cancers. A woman in the U.S. have one out of eight chance of developing breast cancer sometime in her life. Moreover, around 252,710 new cases of invasive breast cancer will be diagnosed in women and approximately 40,610 women will die from this cancer.
Find more information about breast cancer at CancerCauses.news.
Sources include:
Tagged Under: breast cancer, cancer risk, estrogen levels, excess fat, obese, obesity, overweight, women's health