07 July 2017

Stop colorectal cancer

Scientists have found out how to protect yourself from the development of rectal cancer

RIA News

Rectal cancer resulting from a fatty diet can be suppressed by blocking the work of the STRA6 protein associated with vitamin A transfer and stem cell growth and reproduction, according to an article published in the journal Cell Stem Reports (Karunanithi et al., RBP4-STRA6 Pathway Drives Cancer Stem Cell Maintenance and Mediates High-Fat Diet-Induced Colon Carcinogenesis).

"We have known for a long time that diet has a very strong effect on the development of rectal and colon cancer. Now, for the first time, we have managed to find a real link between fatty foods and the development of cancer by identifying a specific molecular chain that is responsible for the formation of its cells. Now we can start creating drugs that block it and reduce the risk of developing cancer," said Matthew Kalady from the Cleveland Clinic (in a press release, Cleveland Clinic Researchers Publish New Findings on the Influence of High–Fat Diet on Colorectal Cancer - VM).

Cancer of the rectum and colon, along with heart and vascular diseases, is now considered one of the main causes of death in developed countries in old age. According to statistics from the World Cancer Research Foundation (WCRF), every year this type of cancer is diagnosed in almost 1.5 million men and women, about 10-20% of whom die due to complications or metastases. 

Recent studies show that obese people and people who eat a lot of fatty and high-calorie foods are more likely to suffer from rectal cancer and other types of malignant tumors of the gastrointestinal tract. For this reason, biologists have been looking for chains of genes and proteins for a long time that can cause intestinal stem cells, whose number in the body of animals and humans increases sharply when eating fatty foods, to mutate and "rebel".

Calady and his colleagues discovered the first such chain directly related to a set of JAK2-STAT3 genes that cause cancer by conducting experiments on mice in whose intestines cancer cells were implanted. Biologists fed rodents with normal and high-calorie food and monitored how fast the tumors grew, and simultaneously observed changes in gene activity in cancer and "normal" intestinal cells.

These observations helped to find out that the STRA6 protein, which usually plays the role of a transporter of vitamin A molecules, plays a key role in the development of cancer and the survival of "rebellious" cells in the early stages of tumor existence. Its molecules, as Calady and his colleagues found out, attach to special receptors on the surface of future cancer cells and force them to "turn on" JAK2-STAT3 and several other genes associated with this system, which usually work inside stem cells and cause them to multiply. Sooner or later, this leads to the fact that STRA6 "turns on" not a healthy stem cell, but a mutated cell with damaged DNA, and thereby initiates the birth of a tumor.

According to scientists, STRA6 is not the only carrier of vitamin A in the body, which prompted them to the idea of whether it is possible to block it to reduce the likelihood of developing cancer. After doing this procedure on mice, biologists found that tumors began to grow much more slowly, and the chances of their development in the body of healthy rodents when eating fatty foods decreased markedly.

Moreover, the "shutdown" of STRA6 in cancer cells actually condemns the tumor to death, since its cells almost completely cease to multiply and resist the attacks of the immune system. All this suggests that drugs that block the work of this protein can be used in the future to fight cancer of the rectum and colon, according to Calady and his colleagues.

Portal "Eternal youth" http://vechnayamolodost.ru  07.07.2017


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