NHRI Deciphers MYADM Protein as Key Driver in Cancer Metastasis Mimicking White Blood Cells
A research team at Taiwan's National Health Research Institutes (NHRI) has discovered that cancer cells mimic the amoeboid migration of white blood cells to metastasize, with the transmembrane protein MYADM identified as a critical driver. Overexpression of MYADM is linked to cancer malignancy and reduced patient survival in various cancers. The team has initiated preliminary development of MYADM-targeting monoclonal antibodies and proteolysis-targeting chimeras (PROTACs), and suggests MYADM as a potential biomarker for RhoA inhibitors. This research was published in the journal "Cancer Research" last year.
📋 Article Processing Timeline
- 📰 Published: April 13, 2026 at 16:21
- 🔍 Collected: April 13, 2026 at 16:31 (10 min after Published)
- 🤖 AI Analyzed: April 13, 2026 at 18:29 (1h 57m after Collected)
The National Health Research Institutes (NHRI) announced on April 13, 2026, a significant breakthrough in cancer research. The team, led by Dr. Dai-Lung Cha, Distinguished Investigator and Director of NHRI's National Institute of Cancer Research, and Assistant Professor Yi-Ta Tsai from National Defense Medical Center, found that cancer cells adopt an amoeboid-like migration strategy, similar to white blood cells, to spread to distant organs. This process, responsible for 90% of cancer-related deaths, is driven by the overexpression of the transmembrane protein MYADM. Their study, published last year in "Cancer Research," a journal of the American Association for Cancer Research, is the first to link MYADM expression to cancer malignancy in human cells. The researchers developed an "LTAG score" based on Leukocyte Migration Associated Genes and identified MYADM as the most predictive gene among 1400 regulatory genes. High MYADM expression was significantly correlated with increased postoperative recurrence and decreased patient survival in breast, kidney, lung, and lymphoma cancers. In mouse models, inhibiting MYADM protein expression reduced cancer cell invasiveness and induced apoptosis. Mechanistically, overexpressed MYADM activates RhoA protein, facilitating cell membrane protrusions and enhancing cancer cell survival in circulation, thereby increasing metastasis. The findings suggest MYADM's potential as a biomarker for existing RhoA inhibitor drug development.