Researchers have found a way pancreatic cancer cells evade immune detection, potentially paving the way for new treatments. This cancer, particularly aggressive, is known for its ability to grow quickly without triggering a response from the body’s immune system.
An international team led by the University of Würzburg has discovered what they call a “molecular invisibility switch.” The team’s study reveals that a protein called MYC, known for promoting cell growth, can also suppress immune signaling. This finding was published in the journal Cell.
Typically, MYC drives cell division by binding to DNA. However, under stress, it switches function, moving from DNA to RNA. In this state, it forms clusters around RNA-DNA hybrids, which are structures known as R-loops.
The study highlights that MYC has several RNA-binding regions. One region, RBRIII, plays a crucial role by attracting an RNA-degrading complex to break down abnormal RNA, preventing immune system activation.
Normally, RNA-DNA hybrids can trigger immune responses through pathways involving receptors like TLR3. The researchers found that MYC, via RBRIII, prevents such pathways, stopping the immune system from recognizing the cancer.
In experiments on mice, only tumors with fully functional MYC continued to grow substantially. Mutations in the RBRIII region led to tumor shrinkage, but only in mice with working immune systems.
These findings suggest that while MYC’s role in cell growth is intact, its ability to hide tumors from the immune system can be disrupted. This could enable treatments that expose cancers to immune attack without damaging other MYC functions.
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