Cancer as we age becomes even more aggressive due to molecules in the blood

A molecule that accumulates in the blood of older people through the metabolism of proteins and fats may promote cancer in old age. It gives cancer cells the ability to spread from one place in the body to others and therefore form metastases. In their study, researchers report that methylmalonic acid (MMS), which is a byproduct of protein and fat digestion, thusSpread of tumorsenabled.

Why does the risk of cancer increase with age?

As people age, the risk of developing cancer increases because people accumulate genetic mutations and are constantly exposed to cancer-causing substances. Most cancer-causing agents are found in the environment, but some are produced by the body. MMS is found in very small amounts in the blood cells of young people. Normally, this binds to the coenzyme A molecule to form methylmalonyl coenzyme. In a reaction it is then converted into succinyl coenzyme. Vitamin B 12 also takes part in this as a cofactor. The succinyl-CoA then enters the tricarboxylic acid cycle. This is a series of chemical reactions that is an essential part of producing energy in the cell. In some diseases, the body cannot metabolize MMS efficiently, resulting in toxic buildup in the blood. The metabolic disorder methylmalonic acidemia occurs, for example, due to failed conversion of methylmalonyl-CoA to succinyl-CoA due to genetic defects in key enzymes orVitamin B 12-Deficiencyon.

In addition, the researchers report that levels of methylmalonic acid in the blood of healthy people over 60 are significantly higher than in people under 30. The increased MMS level also did not cause any cancer in the people examined. However, the authors found that treating human cancer cells with serum from the older group's blood or with high concentrations of MMS caused them to acquire characteristics of metastatic cancer cells. These are those that can spread from a primary tumor to semen cancer elsewhere in the body. These features include a loss of cell-cell binding and an increase in mobility. When injected into laboratory mice, the cells formed metastatic tumors in the lungs.

Study results

All subjects in this study who had high MMS plasma levels appeared to be cancer-free. This suggests that the effects of the molecule are due to the spread of cancer in the body rather than the initial cancer development. Cancer development and spread are different processes that involve different molecular mechanisms. Future studies could confirm whether MMS specifically affects metastasis in humans in the same way. This molecule is different from many previously known age-related causes of cancer, including environmental factors and genetic mutations. Further investigation into the timing of MMS action could then determine the optimal time for therapeutic use of MMS inhibitors if they become available.

A final question is how MMS stimulates changes in gene expression associated with metastasis at the molecular level. The authors of the study hypothesized that MMS activates the transcription of the TGF-β2 gene. However, it remains to be seen how MMS enhances this transcription. Answers to these questions will advance understanding of metabolic changes and their role in cancer development. Regardless of the answersthe Studybroadened the view of cancer risk factors by drawing attention to the role of metabolism in age-related cancer development.