"Junk DNA" is about aging and cancer

"Junk DNA" is about aging and cancer

"Junk DNA" is about aging and cancer "Junk DNA" is about aging and cancer

DNA illustration stock image

 DNA illustration stock image

The human body is essentially composed of trillions of living cells
.

Therefore, when the cells eventually stop replicating and dividing, the human body will age as the cells age

In a study recently published in the Proceedings of the National Academy of Sciences, Washington State University School of Pharmacy Professor Zhu Jiyue (transliteration) led a team to discover a DNA region named VNTR2-1, which seems to drive the telomerase gene The activity of this gene has been shown to prevent certain types of cell senescence
.

The telomerase gene controls the activity of telomerase, and telomerase helps produce telomeres.
Telomeres are the "caps" located at the end of each DNA chain and protect the chromosomes in people's cells
.

In normal cells, the length of telomeres shortens a little every time DNA is copied before the cell divides

However, in certain cell types—including germ cells and cancer cells—the activity of the telomerase gene ensures that telomeres are reset to the same length when the DNA is replicated
.

The author stated that, in essence, this is the reason for restarting the aging clock in new offspring, but it is also the reason why cancer cells can continue to multiply and form tumors

Understanding how the telomerase gene is regulated and activated, and why it is only active in certain types of cells, may one day become the key to understanding how humans age and how to prevent the spread of cancer
.

For this reason, Zhu Jiyue has only focused on studying this gene in her scientific career in the past 20 years

Zhu Jiyue said that his team recently discovered that VNTR2-1 helps drive the activity of the telomerase gene
.

This finding is particularly noteworthy because of the type of DNA sequence it represents

"Almost 50% of the human genome is composed of repetitive DNA that does not code for proteins
.

" He said, "These DNA sequences are often considered'junk DNA' or dark matter in the human genome, which is difficult to study

Based on a series of experiments, they found that deleting the DNA sequence of cancer cells (whether human cell lines or mice) can shorten telomeres, cell senescence, and tumors stop growing
.

Subsequently, they conducted a study to observe the length of the DNA sample sequence of the control group participants in the study of Caucasian and African American centenarians and Georgia centenarians

"It's very different
.

In fact, our research shows that the telomerase gene is more active in people with longer sequences

Since very short sequences were only found in African-American participants, they observed this group more closely and found that compared with the control group participants, there were relatively fewer centenarians with shorter VNTR2-1 sequences
.
However, Zhu Jiyue said that it is worth noting that a shorter sequence does not necessarily mean a shorter lifespan, because it means that the activity of the telomerase gene is lower and the telomere length is shorter, which may reduce the possibility of cancer.

.

"Our findings indicate that the VNTR2-1 sequence contributes to the genetic diversity of aging and cancer
.
" He said, "We know that oncogenes (or cancer genes) and tumor suppressor genes do not explain all the reasons why people get cancer
.
We The research shows that this situation is much more complicated than the mutation of cancer-causing genes, which shows that we should expand our research and study this so-called junk DNA more carefully
.
"

Zhu Jiyue pointed out that because African-Americans have lived in the United States for several generations, many of them have white ancestors and may have inherited some related gene sequences from whites
.
In the next step, he and his team hope to study this sequence in African populations
.
(Source: Feng Weiwei, China Science News)

Related paper information: https://doi.
org/10.
1073/pnas.
2019043118

https://doi.
org/10.
1073/pnas.
2019043118