June 16, 2024

Novel Genetic Mechanisms Discovered in Glioma Cells: A New Approach to Therapeutic Targeting

New research from the lab of Shi-Yuan Cheng, Ph.D., professor in the Division of Neuro-oncology at the Ken and Ruth Davee Department of Neurology, has uncovered novel mechanisms related to RNA splicing within glioma tumor cells. These mechanisms could potentially serve as new therapeutic targets against this type of brain tumor, according to a study published in the Journal of Clinical Investigation.

Xiao Song, MD, Ph.D., research assistant professor of Neurology and the study’s lead author, shares, “We’ve discovered a new way to approach treating glioma through the alternative splicing perspective. We’ve identified some novel targets that have not been identified before but are crucial for glioma malignancy.”

Gliomas are the most frequent primary brain tumors in adults, originating from glial cells that support neurons in the central nervous system. These tumors are highly resistant to standard treatments like radiation and chemotherapy due to their genetic and epigenetic diversity, making the discovery of new therapeutic targets essential.

Previous research from the Cheng lab, published in Cancer Research, revealed that an essential splicing factor, SRSF3, is significantly overexpressed in gliomas compared to normal brains. SRSF3-regulated RNA splicing promotes glioma growth and progression by influencing various cellular processes within the tumor cells.

RNA splicing is a process where introns (non-coding regions of RNA) are removed, and exons (coding regions) are spliced back together to form a mature strand of messenger RNA, supporting gene expression within the cell.

In this study, the researchers aimed to identify alternative splicing changes in glioma tumor cells, understand the mechanisms behind these alterations, and assess their potential as therapeutic targets.

1. Source: Coherent Market Insights, Public sources, Desk research
2. We have leveraged AI tools to mine information and compile it