Novel Study Identifies Enzyme SMYD3 as a Potential Target in Prostate Cancer Progressio

Novel Study Identifies Enzyme SMYD3 as a Potential Target in Prostate Cancer Progression

VoM News Desk | December 26, 2023 | 01:00 PM IST | Breaking News, Health, United States of America | Follow on Google News

Novel Study Identifies Enzyme SMYD3 as a Potential Target in Prostate Cancer Progression

Novel Study Identifies Enzyme SMYD3 as a Potential Target in Prostate Cancer Progression

Prostate cancer ranks as the second most diagnosed cancer in men after skin cancer, with approximately 288,000 new cases annually, according to the American Cancer Society.

Despite a notable decrease in fatality rates since the 1990s, advancements in managing or preventing aggressive metastatic disease are still required to further reduce fatalities associated with the condition.

A recently published study in Science Advances sheds light on the potential role of an enzyme known as SMYD3 in the progression of prostate cancer toward a more dangerous and aggressive stage.

This newly uncovered function of the enzyme positions it as a promising target for potential therapeutic intervention to impede disease advancement.

Erin Green, an associate professor of biological sciences at the University of Maryland, Baltimore County (UMBC), and a senior author of the study, emphasizes the considerable interest in understanding the role of SMYD3 in cancer due to its abundant presence in cancerous tumors compared to healthy tissue.

However, the literature on this protein has been somewhat confusing.

Previous studies indicated that SMYD3 functioned within a cell’s nucleus, regulating gene expression by directly modifying DNA.

But recent research led by Nicolas Reynoird suggested an alternative mechanism: SMYD3 might work outside the nucleus, activating a specific protein called a MAP kinase, known for its hyperactivity in cancer cells, potentially fueling tumor growth.

The new Science Advances study, led by Sabeen Ikram, a postdoctoral fellow at Stanford University, builds upon earlier research and clarifies how SMYD3 could potentially trigger metastatic prostate cancer via the MAP kinase signaling pathway. The study in cells and mice indicates that SMYD3’s probable role in promoting metastasis involves the addition of methyl groups to the MAP kinase. Experiments deactivating SMYD3 significantly reduced the likelihood of metastasis.

Remarkably, compounds capable of inhibiting SMYD3 are already available, and initial experiments with one of these inhibitors effectively eliminated cancer cells in a lab setting. Further experiments in mice are being pursued to confirm the compound’s impact. Researchers are also exploring whether targeting SMYD3 could be beneficial for treating cancers that become resistant to other therapies.

Additionally, the study discovered that SMYD3 increased the activity of vimentin, a well-known marker of cancer progression. Green anticipates investigating the broader applicability of this mechanism across various cancer cell types beyond prostate cancer.

The findings open potential avenues for using SMYD3 as a therapeutic target in prostate and other cancers. The existence of SMYD3 inhibitors might incentivize further exploration and development of these compounds for novel applications in cancer therapy. Green highlights the untapped potential of existing drugs and the need for continued research in this promising area.

VoM News Desk

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