Switch ‘turns off’ breast cancer metastasis in mice
Researchers have pinpointed a gene that causes an aggressive form of breast cancer to rapidly grow in animal models and how to "switch it off."
Researchers have identified a gene that causes an aggressive form of breast cancer to rapidly grow in animal models.
More importantly, they have also discovered a way to “turn it off” and inhibit cancer from occurring.
The study results have been so compelling that the team is now working on FDA approval to begin clinical trials.
The researchers examined the role two genes play in causing triple negative breast cancer (TNBC).
TNBC is considered to be the most aggressive of breast cancers, with a much poorer prognosis for treatment and survival. The researchers specifically identified an inhibitor of the TRAF3IP2 gene, which they proved suppressed the growth and spread (metastasis) of TNBC in mouse models that closely resemble humans.
Inhibiting the TRAF3IP2 gene not only stopped future tumor growth but caused existing tumors to shrink to undetectable levels.
In parallel studies looking at a duo of genes—TRAF3IP2 and Rab27a, which play roles in the secretion of substances that can cause tumor formation—the research teams studied what happens when they were stopped from functioning.
Suppressing the expression of either gene led to a decline in both tumor growth and the spread of cancer to other organs.
When the researchers silenced Rab27a, the tumor did not grow but was still spreading a small number of cancer cells to other parts of the body, says Reza Izadpanah, an assistant professor of medicine at Tulane University School of Medicine.
When the TRAF3IP2 gene was turned off, however, they found no spread (known as “metastasis” or “micrometastasis”) of the original tumor cells for a full year following the treatment.
Even more beneficial, inhibiting the TRAF3IP2 gene not only stopped future tumor growth but caused existing tumors to shrink to undetectable levels.
“Our findings show that both genes play a role in breast cancer growth and metastasis,” says Izadpanah.
“While targeting Rab27a delays progression of tumor growth, it fails to affect the spread of tiny amounts of cancer cells, or micrometastasis. On the contrary, targeting TRAF3IP2 suppresses tumor growth and spread, and interfering with it both shrinks pre-formed tumors and prevents additional spread,” he says.
“This exciting discovery has revealed that TRAF3IP2 can play a role as a novel therapeutic target in breast cancer treatment.”
The team is now working on getting FDA approval and hopes to begin clinical trials soon.
The research appears in the journal Scientific Reports . Additional researchers from Tulane University and the University of Missouri contributed to the work.
Source: Tulane University
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