Metastasis of triple-negative breast cancer (TNBC) could be prevented through the novel use of a class of drugs previously approved by the US Food and Drug Administration (FDA), according to results from research in cell culture and mouse xenograft models.1
A protein called SNAIL is involved in cancer metastasis and is regulated by CDK4/6. CDK4/6 is an important drug target, and its inhibition could prevent metastasis in triple-negative breast cancer.
Inhibitors of CDK4/6 have been approved for the treatment of estrogen-positive breast cancer but not for the treatment of TNBC.
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“Metastasis is a hallmark of cancer and a leading cause of cancer death,” said senior author, Zhenkun Lou, PhD, a faculty member in the department of oncology at the Mayo Clinic, Rochester, Minnesota.
“Despite great progress in cancer therapy, the prevention of cancer metastasis is still an unfulfilled challenge.”
Researchers focused on TNBC, which is difficult to treat as it lacks receptors for estrogen, progesterone, and HER-2/neu. Many current therapies target the receptors that TNBC lacks.
“Our data confirmed that, while the rate of growth of triple-negative breast cancer was not affected by CDK 4/6 inhibitors, this class of drugs was able to significantly inhibit the spread of triple-negative breast cancer to distant organs when tested in multiple different triple-negative breast cancer models, including patient-derived xenografts,” explained Dr Lou.
More research is needed. If these results are confirmed, the use of CDK4/6 inhibitors could expand, potentially including prevention of metastasis in other types of cancer that have high levels of SNAIL protein.
New studies focusing on the role of CDK 4/6 inhibitors and their potential to inhibit metastasis in women with TNBC who are at highest risk for metastasis are currently in development.
Reference
1. Liu T, Yu J, Deng M, et al. CDK4/6-dependent activation of DUB3 regulates cancer metastasis through SNAIL1. Nat Commun. 2017 Jan 9. doi: 10.1038/ncomms13923.
