RNA Cancer Therapy – That Silences KRAS and MYC Genes
Researchers at the University of North Carolina Lineberger Comprehensive Cancer Center have developed a potent RNA-based molecule that can silence two of the most challenging cancer-related genes, KRAS and MYC, at the same time. This “two-in-one” molecule targets both genes and delivers drugs directly to tumors that express them. The discovery opens a new path forward in treating aggressive cancers that have long resisted conventional therapies.
KRAS and MYC: Why These Genes Matter
KRAS and MYC are among the most well-known cancer drivers. KRAS mutations appear in about 25% of all human cancers, including some of the most common and deadly types like lung, pancreatic, and colorectal cancers. MYC is overactive or dysfunctional in 50–70% of cancers, yet no approved drugs have successfully targeted it so far.
These two genes often work together to promote tumor growth by fueling inflammation, blocking cell death, and activating survival mechanisms. Because they reinforce each other, shutting down both could severely impair cancer cell function.
A Two-in-One RNA Molecule with Big Impact
The UNC team used inverted RNA interference (RNAi) technology to design a molecule that delivers small interfering RNAs (siRNAs) capable of disabling both KRAS and MYC. In lab tests, this approach showed up to a 40-fold improvement in reducing cancer cell survival compared to targeting one gene at a time.
This represents the first known molecule to co-silence both KRAS and MYC—a strategy that significantly amplifies therapeutic effects. The combined targeting weakens tumors on multiple fronts, reducing their ability to resist or adapt to treatment.
Beyond KRAS G12V: A Broader Approach
This research builds on earlier work by the same team, which focused on a delivery system for a specific KRAS mutation—G12V. While that method was mutation-specific, the new molecule can target all common KRAS mutations, making it useful for a broader range of patients.
This matters especially in cancers where KRAS mutations are dominant, such as:
- ~30% of lung adenocarcinomas
- ~40% of colorectal cancers
- ~90% of pancreatic cancers
These three cancers alone account for almost 500,000 new cases each year in the United States.
Design Flexibility for Personalized Therapy
One of the most promising features of this RNA molecule is its modular design. It can be adapted to silence different pairs of genes or even three or more targets at once. This offers potential for treating tumors with complex genetic profiles, where multiple mutations drive disease progression.
Targeting more than one gene simultaneously reflects the reality of how cancers function. Most tumors rely on multiple gene abnormalities to grow, survive, and resist drugs. This technology aims to match that complexity with multi-targeted, precision treatment.
A New Chapter for RNA-Based Cancer Therapeutics
RNA-based treatments are gaining momentum, especially after the success of mRNA vaccines. This breakthrough from the University of North Carolina strengthens the case for RNA therapeutics as a viable, scalable option in cancer care.
By using RNA molecules to block disease-causing genes directly, researchers are now able to reach targets that small-molecule drugs cannot. This approach may soon allow clinicians to personalize treatment based on the genetic makeup of each patient’s cancer.
Next Steps Toward Clinical Use
The research team is now preparing for preclinical testing in animal models and planning future steps toward clinical trials. If proven safe and effective in humans, this new RNA platform could transform treatment options for patients with KRAS- and MYC-driven cancers, who currently face limited therapeutic choices.
This discovery not only advances the understanding of how to disable key cancer genes but also demonstrates the potential for multi-gene RNA therapies. With further development, it could help shift the standard of care toward precision, gene-based cancer treatment.
