Source: Journal Of Cell Biology Jul 13, 2018 6 years, 5 months, 6 days, 2 hours, 58 minutes ago
Scientists have found it challenging to understand why some breast cancers become resistant to drugs. A recent study concludes that a sticky protein might be the answer.
Fibronectin:A glue-like protein may help to explain
breast cancer drug resistance.
The hormone
estrogen plays a vital part in the development of
breast cancer.
An estimated 70 percent of all breast cancers are estrogen receptor (ER)-positive.
Put simply, this means that estrogen is the driver of cancerous cell growth in these individuals.
Usually, the hormone attaches itself to estrogen receptors and encourages healthy cell growth. However, increased activity from these receptors can also fuel breast cancer.
While researchers are well aware of estrogen's role, they have failed to solve a particular problem when it comes to treatment.
People who have an ER-positive form of breast cancer are usually prescribed drugs to stop it from spreading. These work by either lowering estrogen levels or hindering receptor activity.
But, approximately one third of people treated using endocrine therapy become resistant to the drugs and are, therefore, less likely to benefit.
Discovering fibronectin
A new study might have found a reason for this drug resistance. Carried out by Rocío Sampayo, a Ph.D. student based at the Instituto de Nanosistemas, Universidad Nacional de San Martin, and Instituto de Oncología "Angel H. Roffo," Universidad de Buenos Aires — both in Argentina — it examined the influence of a glue-like protein called fibronectin.
This substance forms part of a network of proteins and molecules that surround cells. Cancerous cells seek and take over nearby tissue, thereby coming into contact with the fibronectin protein.
The study found that when cancerous cells were exposed to fibronectin, the activity of estrogen receptors was boosted.
The reason for this could be relatively simple. In a normal cell, estrogen receptors are often "eaten up" by lysosomes, but in a breast cancer cell, they are protected by fibronectin and continue to promote growth.
How can this help?
Sampayo thinks that fibronectin could be the missing puzzle piece that allows
"breast cancer cells to become resistant to common endocrine therapy drugs that target the receptor."
By developing a drug that can affect the relationship between the protein fibronectin and estrogen receptors, drug-resistant breast cancers could become a thing of the past.
This is likely to take some time an
d will require further research before concrete conclusions can be made. However, these findings might be the key to a novel form of
cancer treatment.
Reference: Journal Of Cell Biology
