Researchers discover breakthrough to halt rare kidney cancer

Published in Nature Communications, the study reveals that RNA molecules, normally serving as messengers, are hijacked by cancer cells to form liquid-like droplet hubs in the nucleus. These hubs act as command centers that activate genes promoting rapid tumor growth.

Turning off tumor “Droplet Hubs”

The research team engineered a molecular switch capable of dissolving these droplets on demand, effectively halting tumor progression in both lab and animal models. The cancer is driven by TFE3 oncofusions, hybrid genes formed when chromosomes fuse abnormally.

“RNA is not merely a messenger—it’s an active participant that helps build these condensates,” said Dr. Yun Huang, Professor at the Texas A&M Institute of Biosciences and Technology. The team also pinpointed an RNA-binding protein, PSPC1, that stabilizes the droplets, enhancing cancer’s ability to grow.

Advanced genetic tools and targeted therapy

Using CRISPR gene editing and next-generation sequencing, researchers mapped how TFE3 oncofusions interact with RNA to create these hubs. They then built a nanobody-based chemogenetic tool — a precise “off switch” that dissolves the droplets and blocks cancer spread.

“This finding opens the door to a new class of targeted therapies that are both effective and less toxic,” said Dr. Yubin Zhou, Director of the Center for Translational Cancer Research.

Hope for broader cancer applications

Because many childhood cancers are driven by similar fusion proteins, scientists believe this strategy could extend to other aggressive tumors.

“By learning how these proteins engage with RNA, we’re revealing weak points that can be exploited for treatment,” said Dr. Lei Guo, Research Assistant Professor at the Institute.

Translocation renal cell carcinoma accounts for around 30% of renal cancers in children and adolescents, where treatment options are still limited. This breakthrough offers new hope for young patients and families battling this devastating disease.