New Drug May Stop Cancer Cell Growth By Targeting This GeneC. Dixon
Two related studies have shown promising results in testing a new drug targeting a specific, cancer-related gene. The gene, called c-Myc, is associated with obesity and can trigger both lung and breast cancer.
The drug, I-BET-762, can keep existing cancers from continuing to grow and spread, and also helps prevent precancerous cells from becoming cancerous.
What does the gene do?
That’s because it is responsible for a lot. c-Myc can control cell growth and proliferation, cell progression, cell adhesion and differentiation, DNA replication, and metabolism. It is heavily associated with obesity, and since 20% of cancers are estimated to be caused by obesity, understanding this gene is especially important. When an obese person has excess adipose tissue concentrated around their organs (called visceral fat) rather than large amounts of the subcutaneous fat found underneath the skin, their risk increases for a variety of cancers, including breast cancer.
Visceral fat can trigger an overexpression of the c-Myc gene, which, in turn, can make cells cancerous. Researchers at Michigan State University decided to study the gene’s response to the drug I-BET-762, to see if it affected already-existing cancers and precancerous cells.
The first study
Karen Liby, associate professor in the Department of Pharmacology and Toxicology at Michigan State University, led the preclinical study. They focused on I-BET-762’s ability to stop or slow the growth of already-existing tumors, and the results were released in the publication Cancer Prevention Research.
I-BET-762 is a bromodomain inhibitor that has anti-inflammatory effects. It affects the ability of BET (bromodomain and extraterminal proteins) to bind to specific proteins, and halts cell growth.
“I-BET-762 works by targeting DNA so that this gene can’t be expressed,” Liby said. “It does this by inhibiting a number of important proteins – both in cancer and immune cells.”
It stopped the growth of proteins pSTAT3 and pERK in tumor cells by targeting the c-Myc gene, and also had an effect on immune cells in different organs.
Because these proteins are important for both immune cells and cancer cells to function, stopping their growth is crucial. For example, when the protein pSTAT3 is activated in immune cells, it can prevent the cells from attacking cancerous cells. When overproduced in cancer cells, this same protein acts as a “shield” and protects the tumor from being attacked.
During the study, pSTAT3 levels fell by 50% in both immune cells and cancer cells, which cut the amount of cancer cells overall by 80% in mice.
The Second Study
Liby’s colleague, Jamie (J.J.) Bernard, also an assistant professor at MSU, took what Liby had discovered in her study and used the drug on precancerous cells — ones that “could become tumorigenic, but weren’t quite yet.”
I-BET-762 prevented more than 50% of those cells from actually becoming cancerous.
Reducing mortality rates for breast cancer has been mostly unsuccessful so far, but drugs similar to I-BET-762 are being tested in multiple clinical trials against a variety of cancers. The hope is that these types of drugs will help increase overall survival rates by attacking both the precancerous cells and the cells that have already become cancerous.
“The goal is our findings will clarify what needs to be targeted and therefore, can be used to prevent cancer in high-risk patient populations,” Bernard said.
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