Targeting the MYC Protein: A New Frontier in the Fight Against Cancer

For decades, medical researchers have been locked in an intricate battle against cancer, primarily focusing on the mutated proteins that drive tumor growth. Yet, cancer’s adaptability has posed significant challenges, as it can often find ways to circumvent such targeted interventions. A groundbreaking strategy is now emerging from the University of California, San Francisco (UCSF), aimed at a critical protein called MYC, implicated in roughly 70% of all cancers.

MYC stands out among cancer-driving proteins because it is infrequently mutated. Its impact arises from overexpression, leading to rapid and uncontrolled tumor growth. This has been a known fact since its discovery by Nobel laureates at UCSF in the 1970s. The problem has always been that MYC’s hyperactivity, without mutation, makes it a challenging target for standard cancer therapies.

Enter Dr. Joanna Kovalski and her innovative team at UCSF. They have shifted the focus from altering MYC’s genetic foundation to stopping its production altogether. Central to their breakthrough is a protein called RBM42, pivotal in the translation process of converting MYC mRNA into the MYC protein. This translation process is crucial for the unchecked proliferation of cancer cells.

Their study highlights a significant discovery: by targeting RBM42, particularly in cases of pancreatic cancer—a notably aggressive and hard-to-treat cancer type—the synthesis of MYC can be dramatically reduced. Without MYC, cancer cells lose their growth advantage and begin to perish, offering the potential framework for a novel class of cancer therapies.

RBM42’s function in preparing and transporting MYC mRNA to ribosomes—the cellular machinery responsible for protein synthesis—plays a vital role. Disrupting this pathway by inhibiting RBM42 compromises the cancer cells’ ability to produce MYC. These promising results, obtained both in laboratory conditions and in animal models, underscore RBM42’s critical role as a facilitator of MYC overproduction.

This discovery holds significant implications for future cancer treatment strategies. By targeting the synthesis of MYC, rather than mutations within the MYC gene itself, researchers are laying the groundwork for interventions that could potentially halt cancer progression in its tracks.

The UCSF team’s work emphasizes the therapeutic potential of focusing on the protein synthesis pathway. Instead of conventional genetic modification techniques, controlling the translation process opens new avenues for cancer therapy. This approach offers hope for creating more effective treatments against some of the most resilient and deadly forms of cancer, such as those affecting the pancreas. Overall, UCSF’s research represents a promising leap forward, harnessing novel mechanisms to combat cancer and offering hope for future advancements in the field.