Dallas (TCA/DPA) – Fat is not just a pleasure of guilt – it is a secret weapon of cancer. New research on the UT Southwest Medical Center explains why this is the case.
In a study published this month, Nature researchers found that cancer cells steal fat -packed molecules from the bloodstream, armed with a strong antioxidant that protects them from death.
Tumors seem to do this by wrapping lipoprotein-molecules containing fat and fat soluble nutrients such as vitamin E in the blood-over sugar covered molecules on their cell surface. These sulfate glycosaminoglycans (or GAG) allow cancer cells to strengthen their cell membranes of vitamin E and prevent cellular deaths called ferroptosis.
Although clinical adaptation is still not ways, the study emphasizes how understanding the metabolism of cancer could open a new door for treatment, Dr. Shad Thaxton, an associate professor of urology at the Northwest University of Feinberg, who did not participate in the study.
“I think this document and others outside (emphasizing) the assessment of ferroptosis as a mechanism that reduce cancer cells – that cell death mechanism is so closely intertwined with cell metabolism,” Thaxtton said. “I think people are curious about the fact that metabolism has a great impact on cancer cell vulnerability.”
Building blocks with functional privileges
Cancer overflows its metabolism in a way that supports their growing elastic cells. Part of this switch includes energy production from glucose and cell building blocks such as nucleic acids, proteins and lipids.
The accumulation of cellular building blocks is particularly important, as uncontrolled tumor growth gives it hostile micro-nuclear, where there are not enough nutrients and other resources, said UT Southwestern Medical Center Medical Center Research Institute Javier Garcia-Bermudez.
Lipids are essential for the growth of tumors to grow and progress. The plasma membrane of each cell is a lipid two -layer layer; Because cancer cells swell, they must get lipids from their immediate environment or make their own to maintain their plasma membranes.
Garcia-Bermudez said it was a predominant theory why lipids are so important for cancer. Since then, research has found that lipids can offer cancer cells more functional privileges. For example, in 2024. September The study found that cancer cells use lipids called spyingolipids to move to secret regime, avoiding detection and destruction of the immune system.
Studies also found that lipids somehow engage in ferroptosis, 2012. Detected type of cell death. The Latin word “Portmanteau”, Latin word of iron and apoptosis, the scientific word for the death of cells, ferroptosis occurs when necessarily rust from the inside.
“Oxidants damage lipids that form membranes (of) cells,” Garcia-Bermudez said. “Interestingly, cancer cells tend to produce more oxidants than normal cells,” he added, noting that it was interested in understanding why some cancer is more sensitive to this type of lesion and uses ferroptosis to destroy cancer cells.
Cut GagsKill cancer
Creg survival masters, which are, cancer cells have created ways to prevent ferroptosis. After the reason for the Garcia-Bermudez and its laboratory to be raised on a four-year scientific study trip.
One of the first findings of the researchers, after checking 200 metabolic genes associated with cancer, was that the enzyme, called glutathione peroxidase 4, was active in tumors. This was not a new discovery: research has shown this enzyme, which can stop lipids from humiliation, playing a key role in controlling ferroptosis.
When glutathione peroxidase 4 was deleted from the genome of the cancer cell, the tumor would die – unless he was given a medicine blocking ferroptosis or nourishing lipoproteins.
“It was a hint that lipoproteins were somehow related to ferroptosis,” Dr. Ralph Debrardic, UT Southwestern Medical Center Eugene McDermott Human Growth and Development Center.
In many experiments that included cancer cells from Petri Indoprotein dishes and exposed to different antioxidants, the whole picture was launched. Cancer cells detained lipoproteins from their surrounding environment, especially those containing vitamin E-fat-soluble antioxidant. As a fishing line with a fisherman, cancer cells did not do so with the usual coils used to catch lipoproteins, but with long, flowing sugar chains called sulfates glycaamoglycan (or GAG). These molecules are attached to the surface of cancer cells through another molecule called proteoglycan.
When scientists blocked the biochemical path responsible for GAG production, it restricted the access of a cancer cell in the laboratory to vitamin E and made it more vulnerable ferroptosis. For mice, vaccinated cancer cells, when the road was interrupted, slowed down the growth of the tumor.
Researchers have also examined 20 tumors donated by patients with transparent cell renal carcinoma, the most common type of kidney cancer with more than 640,000 people in the US. These tumors had higher levels of GAG and vitamin E – about 15 times more of the latter – compared to normal kidney tissue. When the biochemical path that causes GAGs, renal cancer cells prevented the swallowing of vitamin e-packere lipoprotein, dying with iron pherroptosis by hand.
Future research
Garcia-Bermudez and Debrarardis Caution that is still needed to do much more studies while their study finds there are any clinical application of cancer.
“We know that the gags are on the surface, they speak with lipoproteins and influence lipoprotein uptake,” Garcia-Bermudez said. “However, how mechanically it happens, especially in the cancer cell, it has not been shown before … If we understand how it works, and we find molecular targets that we may be treated with drugs and block, then we have a way to deplete vitamin E Navike.”
Debrardic said the study shows no connection between diet vitamin E and cancer risk or how vitamin E levels correlate with cancer patient. It would be points for future studies to find out those possible relationships.
In a short period of time, according to the debit, these data could be used to investigate whether tumors with higher levels of glycosaminoglycans or vitamin E are associated with patient results such as survival percentage or how they respond well to treatment.
Thaxton said there are currently no federal -end -of -approved cancer treatments to promote ferroptosis. His laboratory conducts synthetic lipoproteins at the North Western University School of Medicine, without any lipid passengers – Trojan horse, without soldiers, would not hide inside.
Cancer cells expect to get lipoproteins with fat such as cholesterol and vitamin E, Thaxton said, but “they eventually die of ferroptosis. Our medicine does nothing and it is through this mechanism you can kill a cell.”
Garcia-Bermudez and their debit’s research efforts were like finding a needle in a haystack, which they expect to find more needles.
“Our study is really exciting, but at the same time it is a very simple discovery,” Garcia-Bermudez said. “It was incredible to discover what people have noticed before understanding why these tumors are so resistant. I am very happy to continue working.”