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Alternative RNA splissing is similar to cutting and re -arranging a film editor from the same video to produce different versions of a film. By deciding which sequence and which cuts to cut, the editor can make a drama, a comedy, or even a thriller with the same raw material.
Similarly, cells divide RNA in different ways to create a wide range of proteins from the same gene, fixing their activity to meet specific requirements. However, when the cancer writes the script again, this process is interrupted, promotes tumor growth and existence.
RNA Splissing Role in Cancer Development
In a recent study, scientists of Jackson Laboratory (Jax) and Uconn Health not only showed how cancer kidnapped this tightly regulated splissing and RNA, but also introduced a potential medical strategy that could slow down or shrinking aggressive and hard-to-treat tumors. The discovery can change how we treat aggressive cancer such as triple-negative breast cancer and some brain tumors, where current treatment options are limited.
In the heart of this work, under the leadership of Olga Anskuo, Jacks-NCI, an associate professor in Jacques and Jackson Cancer Center, is the co-program leader, small genetic elements called poison exon, the nature’s own “off switch” for protein production. When these exons are included in an RNA message, they trigger its destruction before making a protein-applying hasty cellular activity. In healthy cells, poison exons regulate the major protein levels, keeping genetic machinery under examination. But in cancer, this security system often fails.
Anczukow and his team, including Nathan Lakelair, a MD/PHD graduate student in Uconn Health, and Jackson Laboratory, who led the research, and Matia Brugiio, an employee researcher who contributed his expertise, found that the cancer cells found that the cancer cells suppressed the poisoning activity in a significant gene. For example, the TR2B protein levels grow inside cancer cells, causing tumor proliferation.
In addition, the team found a relationship between poison exon and patient result levels. “We have shown for the first time that the low levels of poison exon inclusion in the Tra2B genes are associated with poor results in many different cancer types, and especially in aggressive and hard-to-treatment cancer,” Anczukow said. These include breast cancer, brain tumors, ovarian cancer, skin cancer, leukemia and colorectal cancer, explained by ANCZUKOW.
Anczukow, Leclair, and Brugiolo noticed if they could increase the poison in the Tra2b gene and increase the Kill switch to activate. He found his reply in the Antheses Oligonucleotides (ASOS)-Skinhetic RNA pieces that could be designed to increase poison exon inclusion in specific ways. When introduced into cancer cells, the ASOS effectively flipped the genetic switch, leaving the body’s natural ability to degrade the excess Tra2b RNA and to inhibit the progression of the tumor.
“We found that ASOS could promote rapid poison exon inclusion, essentially the cancer cell can trick the cell to shut down its own growth signals,” Lakelair said. “These poison exon acts like a rostat, which quickly adjusts protein levels-and it can make ASOS a highly accurate and effective therapy for aggressive cancer.”
Interestingly, when researchers completely removed the Tra2b protein using CRISPR gene editing, the tumor continues to grow-targeting RNA instead of the protein can be a more effective approach. Anczukow explained, “This tells us that RNA-containing poison-aczon doesn’t just silence the Tra2B.” “It is likely that there is a sequence of other RNA-binding proteins, leading to even more toxic environment for cancer cells.”
Further studies will refine ASO-based treatments and detect their delivery for tumors. However, initial data suggests that ASOS are highly specialized and do not interfere with normal cellular functions, making them promise candidates for future cancer treatment.
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