ZMYND8 protein is able to inhibit the expression of tumor metastasis-related genes

Although this protein reads like a license plate number in European countries very much, ZMYND8 protein has been shown to have the effect of inhibiting metastasis of prostate cancer-related genes. The findings mainly came from the research on cell study and recombinant mouse proteins, and they were published online on July 28th in the journal Molecular Cell.

"These findings are quite important because metastasis is a complex process, and studying tumor metastasis is a big challenge for doctors." Dr. Min Gyu Lee is an associate professor of molecular and cellular oncology. He said, "Tumor metastasis is very important. We need to know the key of how tumor cells obtaining the ability of metastasis and invasion. Understanding how this process happens is crucial for doctors to prevent tumor metastasis. We believe that this study could help medical researchers better know and understand the process."

Dr. Lee's research focuses on the modification of proteins using recombinant proteins, and this step is crucial for gene regulation; wherein the acetylation and methylation of tumor development is the most common. Dr. Lee's research group believed that ZMYND8 is the "reader" of histone. Identifying histone modifications is likely to affect gene expression.

"The effect of histone acetylation and methylation on gene expression may receive the impact of specific binding proteins," said Dr. Lee. They found that ZMYND8 is the "reader" of histone marker H3K4mel and H3K14ac, and both of them are related to tumor metastasis-related genes.

The research team also noted that ZMYND8 also has synergy with another type of tumor marker "Eraser" JARID1D. Mutual cooperation between them can inhibit tumor metastasis-related genes. "These findings reveal an unknown mechanism of tumor metastasis suppressor, i.e. ZMYND8 genes can inhibit the expression of tumor metastasis-related genes through reading histone markers H3K4mel and H3K14ad its synergy with JARID1D."

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