Scientists have discovered a key mechanism behind how breast cancer spreads to lymph nodes, identifying a crucial role

for the protein CD36. Their research indicates that elevated levels of CD36 stimulate the Hippo-YAP signaling pathway,

which in turn promotes resistance to anoikis, a form of programmed cell death that normally prevents detached cells from

surviving and metastasizing.

Breast cancer remains a significant global health challenge. According to global cancer statistics, it accounts for a

substantial proportion of cancer diagnoses and deaths worldwide. The process of metastasis, where cancer cells spread

from the primary tumor to other parts of the body, is a major factor in the severity of the disease. Lymph nodes are

often the first site of metastasis for breast cancer cells.

Prior studies have highlighted the importance of metabolic adaptation in cancer progression. Specifically, the ability

of cancer cells to alter their metabolism to survive in new environments is crucial for metastasis. CD36, a scavenger

receptor, plays a significant role in fatty acid uptake and metabolism. It has also been implicated in various cancers,

including breast cancer. Now, new research sheds light on how CD36 influences breast cancer metastasis to lymph nodes.

The Hippo-YAP pathway is a signaling cascade involved in cell growth, proliferation, and survival. When activated, the

YAP protein enters the nucleus and promotes the expression of genes involved in cell survival and proliferation. Anoikis

is a form of programmed cell death that is triggered when cells detach from the extracellular matrix. Cancer cells that

are resistant to anoikis are more likely to survive and metastasize.

This study demonstrates that elevated CD36 levels in breast cancer cells activate the Hippo-YAP pathway. This activation

leads to increased expression of genes that promote anoikis resistance, allowing cancer cells to survive and spread to

lymph nodes. This finding suggests that targeting CD36 or the Hippo-YAP pathway could be a potential therapeutic

strategy to prevent or reduce breast cancer metastasis. Further research is needed to validate these findings and to

develop effective therapies based on this knowledge.