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Scientists Discover Way to Send Information into Black Holes Without Using Energy

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Scientists Discover How Aggressive Triple Negative Breast Cancer Cells Spread In The Body

Triple-negative breast cancer (TNBC) is one of the most aggressive and difficult-to-treat forms of breast cancer. Unlike other breast cancers, TNBC does not respond to hormone therapy or common targeted drugs, leaving patients with limited treatment options. Even more troubling is its strong tendency to spread quickly to other organs — a process known as metastasis, which is responsible for most cancer-related deaths worldwide.

Now, scientists at Baylor College of Medicine have uncovered a surprising strategy that TNBC cells use to spread more efficiently. Their findings, published in Nature Communications, reveal how these cancer cells form protective groups in the bloodstream, helping them survive and establish new tumors in distant organs. This discovery opens the door to new treatment possibilities for patients who urgently need better options.

Understanding Metastasis: When Cancer Cells Travel

Metastasis begins when cancer cells break away from the main tumor and enter the bloodstream. These traveling cells are called circulating tumor cells (CTCs). Once in circulation, they can reach organs such as the lungs, liver, brain, or bones and start new tumors.

Researchers have long known that CTCs are far more dangerous when they move in clusters rather than as single cells. These clusters survive better in blood, resist damage, and attach more easily to new tissues.

“Clusters act like protective teams,” explained Dr. Chonghui Cheng, senior author of the study and professor at Baylor. “They give cancer cells a much higher chance of forming new tumors.”

But TNBC presented a mystery.

Normally, cells stick together using structures called adherens junctions, which act like molecular glue. However, highly aggressive TNBC often loses these junctions. So scientists wondered: If TNBC cells lack this glue, how do they still form strong clusters?

The Discovery of a “Sticky Coat”

To solve this puzzle, Cheng’s team compared TNBC cells with other breast cancer types, including both metastatic and non-metastatic tumors.

One feature stood out: the extracellular matrix, especially a substance called hyaluronan (HA).

The extracellular matrix can be imagined as a soft, sticky coating around cells. It is made of proteins, sugars, and water, and it helps cells stay connected and supported.

The researchers found that TNBC cells produce unusually large amounts of HA. Even more striking, these cancer cells cover themselves in HA, forming a kind of protective outer coat.

This HA is made by an enzyme called HAS2, which TNBC cells produce in high levels.

“When we removed HA from circulating tumor cells, the clusters fell apart,” said Dr. Georg Bobkov, co-first author of the study. “This told us HA is essential for keeping these cells together.”

HA and CD44: A Powerful Partnership

HA does not work alone.

The team discovered that HA attaches to a protein on the cell surface called CD44. CD44 acts like an anchor, holding HA in place and allowing neighboring cells to connect.

Without CD44, HA cannot stay on the cell surface — and without this connection, clustering fails.

Once HA and CD44 link up, another group of proteins called desmosomes strengthens the bond, forming tight but flexible clusters. These clusters are strong enough to survive the harsh forces of blood flow, protecting cancer cells as they travel through the body.

This is especially important because the bloodstream is a hostile environment. Cells experience intense pressure and movement, which would normally destroy them. But clustered TNBC cells are far more resilient.

Flexible Clusters: A Clever Survival Trick

An unexpected benefit of HA-based clustering is flexibility.

Clusters formed through traditional junctions are rigid. In contrast, HA creates clusters that can bend and reshape.

This flexibility turns out to be a major advantage.

When CTC clusters move through tiny blood vessels called capillaries, they often have to squeeze into a single-file line. After passing through these narrow spaces, they regroup.

The researchers finally explained how this happens.

Because HA-mediated clusters are flexible, the cells can temporarily separate, pass through tight vessels, and then reassemble into protective clusters afterward. This ability greatly increases their chances of surviving and spreading.

Recruiting Immune Cells for Protection

The study also uncovered another clever strategy used by TNBC cells: they recruit immune cells for help.

CTC clusters are often mixed with immune cells such as neutrophils. While immune cells usually fight disease, in this case they actually protect cancer cells and promote metastasis.

Neutrophils also carry CD44 on their surface. The HA coating on cancer cells binds to CD44 on neutrophils, pulling them into the cluster.

“These immune cells act like bodyguards,” explained Dr. Khushali Patel, co-first author. “They shield cancer cells and help them survive.”

New Hope for Treatment

Although more research is needed, this discovery opens exciting possibilities for new therapies.

One promising idea is to block the interaction between HA and CD44. If scientists can prevent this binding, CTC clusters may fail to form or fall apart, making cancer cells more vulnerable and reducing metastasis.

Importantly, the researchers also observed HA-CD44 clustering in other cancers, including glioblastoma, prostate cancer, and pancreatic cancer. This suggests that future treatments based on this mechanism could help patients with multiple aggressive cancers.

“For TNBC patients, who currently lack targeted therapies, this finding offers real hope,” said Dr. Cheng.

Looking Ahead

Metastasis remains one of the greatest challenges in cancer treatment. By uncovering how TNBC cells use a “sticky coat” of hyaluronan to form flexible, protective clusters, Baylor researchers have revealed a hidden survival strategy — and a new target for medical intervention.

While clinical treatments based on this discovery are still in development, this research represents an important step toward stopping cancer before it spreads.

For patients facing triple-negative breast cancer, this breakthrough may one day lead to therapies that turn the tide against one of the deadliest forms of the disease.

Reference: Bobkov, G.O., Patel, K.J., Lege, B.M. et al. Extracellular matrix mediates circulating tumor cell clustering in triple-negative breast cancer metastasis. Nat Commun 17, 1352 (2026). https://doi.org/10.1038/s41467-026-69007-w

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