New findings by Taiwanese researchers on the behavior of cancer cells could pave the way for more precise treatments with fewer side effects.
A research team at the National Health Research Institutes (NHRI) found that a transmembrane protein — myeloid associated differentiation marker (MYADM) — is used by cancer cells to activate specific signaling pathways, enabling them to mimic the movement of white blood cells.
This behavior enhances the invasiveness of cancer cells and increases the likelihood of metastasis — the spread of cancer cells from a primary tumor to distant organs or tissues. Targeting MYADM could offer a highly cancer cell-specific treatment approach, potentially allowing for more precise therapies with fewer side effects, the researchers said.
Photo courtesy of the institute
NHRI Cancer Research Institute director Cha Dai-lung (查岱龍) yesterday said that under normal physiological conditions, white blood cells, such as monocytes and neutrophils, migrate using an amoeboid mode of movement.
This involves the formation of spherical membrane protrusions, known as blebs, which allow cells to adapt to dense and complex tissue environments and move efficiently.
Amoeboid migration is a key mechanism by which white blood cells patrol the body and defend against foreign threats, he said.
However, the research team found that cancer cells can “borrow” this mechanism by overexpressing MYADM, which interacts with the regulatory protein RhoGDI. This interaction releases the RhoA protein and converts it into an active state, enhancing cell motility and enabling cancer cells to evade immune surveillance.
The team also found that this mechanism not only drives the formation of membrane protrusions in cancer cells, but also confers resistance to anoikis, a form of programmed cell death that occurs when cells detach from their original environment. This allows cancer cells to survive longer in the circulatory system, increasing the likelihood of metastasis and contributing to disease progression.
Cha said that big data and clinical sample analyses show that high expression of MYADM is significantly associated with higher postoperative recurrence rates and lower survival rates across multiple cancer types, including breast, kidney, lung and lymphoma. Circulating tumor cells were also observed to exhibit particularly high levels of MYADM expression.
Cancer cells with high MYADM expression are highly sensitive to RhoA inhibitors, suggesting that MYADM could serve as a key biomarker for guiding therapies targeting the RhoA pathway, he said.
Suppressing MYADM in cancer cells can also trigger apoptosis without harming normal cells, indicating that targeted therapies against MYADM could provide more precise treatment options with fewer side effects.
The findings were published in 2025 in Cancer Research, a journal of the American Association for Cancer Research.
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