Old age has long been known to be a physiological disease, a major way through which time affects our body mechanics. A lot of persons, who are still young, will rather prefer to just grow old and see more years without actually having to age and get wrinkles. However, so far, the process of aging has remained inevitable and irreversible. Scientists have long studied the genetic cause of aging, its course, and its potential harms or benefits. In a recent development, researchers have unraveled a gene that could have a significant influence on aging- the VNTR2-1, which triggers optimism in the pursuit for ways to halt aging, and cure cancer.
The process of aging
Aging is a natural process that plays out in the background of the continuous division of our cells, and consequent DNA replication. Each strand of our DNA is capped by the telomeres, which guards the chromosomes within our cells, after each DNA replication which leads to subsequent cell division, the length of the telomeres is shortened. The continuous shortening of these telomeres with each DNA replication is the basis of aging, because, when these telomeres are shortened to a certain limit, the DNA could no longer replicate correctly, which results in the aging and death of the cell. However, some cells like the gonadial and cancer cells have a telomerase gene that restores the telomeres to their original state after each DNA replication. This is why cancer cells do not burn out and continue to replicate to form tumors, and why the aging mechanics are refreshed in a newborn.
The telomerase gene regulates the activities of a telomerase enzyme, which reproduces new telomeres to recap the end of the DNA strands of these cells after replication.
A new finding
With fundings from the National Institute of Health’s General Medical Sciences, The Melanoma Research Alliance, and the Health Sciences and Services Authority of Spokane County, researchers at Washington State University were able to dig more into how genetics affects aging, an idea in the science world that was still sketchy.
The team headed by a professor in the College of Pharmacy and Pharmaceutical Sciences, Jiyue Zhu, together with Tao Xu, De Cheng, and other partners at Northeast Forestry University, China, Pennsylvania State University, and North Carolina State University found out that a region in the DNA known as VNTR2-1 gene can influence the telomerase gene. These findings were published in the Proceedings of the National Academy of Science journal, and it revealed how the knowledge of the regulation and activation of the telomerase gene can be insightful in future researches on aging, and stalemating the multiplication and dissemination of cancer cells.
According to Zhu, about half of our DNA is made up of “junk DNA” otherwise dark matters, which are repetitive DNAs that do not transcribe. These genetic dark matters are hard to study. However, it was found that a section of it can positively affect our telomerase gene, because from experiments conducted, erasing the gene from cancer cells in human and mice models caused shortening of the telomeres, aging, and stoppage of growth in the cancer cells.
There is a correlation between the activity of the VNTR2-1 gene, the length of its sequence, and the functionality of the telomerase gene. Junk DNA, oncogenes, and tumor suppressor genes are now known to play a role in cancer pathogenesis, though there is still more to discover. Though this gene may confer an undesirable trait for aging, it also discourages the development of cancer.
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