A new study makes two significant discoveries: firstly, it shows how non-cancerous cells turn into tumorous ones when “helped” by a certain protein, and secondly, it suggests that the source of this protein may lie in the belly fat that so many of us struggle with.
As the authors explain, an established body of research suggests that fat increases cancer risk. However – and despite the rising trends in obesity worldwide – little is known about how fat influences the process by which a non-cancerous cell turns into a cancerous one.
“While there have been several advances in treating cancer and improving the quality of life of patients, the number of new cases continues to surge,” says Prof. Bernard.
And so does obesity. Currently, 38 percent of people in the United States are estimated to be obese, write the authors, and the rates are expected to reach 42 percent by 2050.
“It’s important to understand the cause [of cancer] so we can do a better job at reducing the number of cancer cases using dietary modifications or therapeutic interventions,” says Prof. Bernard.
Specifically, the authors write, it is important to examine in more depth the effect of so-called visceral fat, or visceral adipose tissue (VAT), on cancer development.
Visceral fat is the fat that deposits around several vital organs inside the abdomen, such as the liver, pancreas, and intestines. By contrast, subcutaneous fat is the fat that is stored just under the skin.
Sometimes, this fat is referred to as “active fat,” because, as the authors explain, it does not simply store energy but is also “metabolically active, secreting large numbers of adipokines, cytokines, and growth factors.” In this context, Prof. Bernard and colleagues set out to investigate which factors in VAT promote cancer development in mice.
In order to examine tumor growth in the mice’s epithelial cells and the effects of VAT in vivo, the researchers fed the rodents a high-fat diet, induced cancerous cell formation with ultraviolet B rays, and performed a lipectomy, which is a type of surgery that removes the layer of fat around the waist.
Prof. Bernard and colleagues also developed “a novel system to determine the ability of factors released and filtered from VAT to stimulate cell transformation.”
The researchers found that VAT produced the fibroblast growth factor-2 (FGF2) in much larger amounts when compared with subcutaneous fat.
Additionally, using a proliferation assay, the scientists revealed that FGF2 drives skin and mammary epithelial cells that were “already vulnerable to the protein” to transform into cancerous cells.
Prof. Bernard and team also sampled VAT tissue from women who had undergone a hysterectomy and found that when the fat tissue had higher secretions of the FGF2 protein, more cells went on to form cancer tumors when transplanted into mice.
“This would indicate that fat from both mice and humans can make a non-tumorigenic cell malignantly transform into a tumorigenic cell,” says Prof. Bernard.
Referring to excess weight as a risk factor for cancer, Prof. Bernard says, “Our study suggests that body mass index, or BMI, may not be the best indicator.”
“It’s abdominal obesity, and even more specifically, levels of a protein called fibroblast growth factor-2 that may be a better indicator of the risk of cells becoming cancerous.”
She also points out that other risk factors for cancer should not be ignored.
“There’s always an element of chance in whether a person will get cancer or not. But by making smarter choices when it comes to diet and exercise and avoiding harmful habits like smoking, people can always help skew the odds in their favor.”
Prof. Jamie Bernard
In the future, Prof. Bernard and colleagues plan to find compounds that can halt the effects of FGF2 and inhibit the formation of cancerous tumors.