A new study, made at Baylor College of Medicine in Houston, Texas, gives answers for a long-lasting medical question: how does estrogen influence the cancerous mammalian cell differently one individual from another?
The importance of estrogen in human cells
Estrogen is a hormone known to have a significant influence on mammalian cancer cells. Hormones transmit information and instructions to another’s cell group. In the human body, hormones influence almost every cell, organ, and function.
It regulates the creation, metabolism, function of tissues, sexual function, reproduction, modulation in our caregiving use of food, our body’s response to emergencies, and even our state of mind.
If the interaction between estrogen and mammalian cells can be fully understood and controlled, then illnesses la cancer can be cured.
The research is a new hope
The answer the researchers reached an astonishing answer: estrogen has a different influence on the identical cells of the same individual.
The study reported results from tests made on cells and alleles that were stimulated with estrogen. An allele is a variant form of a given gene. They determined two well-characterized genes, GREB1 and MYC, whose activity is regulated by estrogen. The response on estrogen was asynchronous in both types of cells: some of them reacted, and some of them resisted the estrogen’s attack.
This is called phenotypical heterogeneity. It’s nature’s survival and self-destruction mode. The way cells survive and also get sick. Some survive, and some develop the malfunction.
The researchers investigated multiple reasons that could justify the unexpected heterogeneity. An answer was outlined: MS049, an inhibitor of two proteins, markedly increased the expected number of active alleles per cell under estrogen stimulation, in a gene-specific manner.
The nature of the estrogenic response at the allele level could be altered, indicating that there are ways to prevent maximal and uniform behavior in a population of cells. And this is a first in medical research.