Unlocking the Circadian Code: UCI Scientists Discover Groundbreaking Strategy to Halt Aggressive Breast Cancer

A beacon of hope has emerged in the relentless fight against breast cancer, particularly its most aggressive form. Scientists at the University of California, Irvine (UCI) have unveiled a revolutionary approach that could effectively stop the spread of triple-negative breast cancer (TNBC), a notoriously challenging disease with limited treatment options.

This pivotal discovery centers on manipulating the body's internal clock, offering a promising new frontier in cancer therapy.

Led by Dr. Selma Masri, an assistant professor in the Department of Biological Chemistry, and with postdoctoral scholar Jennifer N. Ho as the first author, the research team identified a critical vulnerability within TNBC cells.

Their findings, published in the prestigious journal Science Advances, highlight the crucial role of the circadian clock protein BMAL1 in fueling the proliferation and metastasis of these aggressive cancer cells.

Triple-negative breast cancer accounts for 10 to 15 percent of all breast cancers and is characterized by its rapid growth, high recurrence rate, and lack of the three most common receptors (estrogen, progesterone, and HER2) that are often targeted by existing therapies.

This makes TNBC particularly challenging to treat, leaving patients with fewer effective options and a poorer prognosis compared to other breast cancer types. The urgency for new, targeted treatments for TNBC cannot be overstated.

The UCI team's breakthrough revealed that the circadian clock protein BMAL1 is not merely a regulator of our sleep-wake cycles but also acts as a powerful metabolic orchestrator within TNBC cells.

They discovered that BMAL1 is essential for these cancer cells to grow and spread. Crucially, by suppressing BMAL1, the researchers were able to significantly block the growth and metastatic spread of TNBC in preclinical models.

This innovative research draws a compelling link between the body's circadian rhythm and cancer metabolism.

It suggests that by targeting BMAL1, scientists can disrupt the very metabolic pathways that aggressive cancer cells rely on for survival and expansion. This mechanistic understanding paves the way for the development of entirely new therapeutic strategies, potentially used alone or in combination with existing treatments, to enhance their efficacy against TNBC.

This discovery represents a significant leap forward in understanding and combating aggressive breast cancer.

The ability to intervene by targeting a core component of the cellular clock system opens up exciting possibilities for improving patient outcomes and offering new hope to those battling this formidable disease. The UCI team's work, supported by organizations such as the National Institutes of Health and the National Breast Cancer Research Foundation, underscores the vital importance of fundamental research in transforming cancer care.