Breaking the MYC Code: A New hope for Halting Cancer’s Deadliest Driver
For decades, scientists have waged war against cancer by targeting mutated proteins in tumors.Yet, many cancers persist, finding ways to outmaneuver these efforts. Now,researchers at UC San Francisco have uncovered a groundbreaking strategy to tackle one of cancer’s most notorious culprits: the MYC protein. Their findings, published in Nature Cell Biology, reveal how disrupting a lesser-known protein, RBM42, can effectively halt MYC production, offering a potential lifeline for patients with aggressive cancers.
The MYC Enigma
MYC, first identified in the 1970s by UCSF Nobel Laureates Michael Bishop and Harold Varmus, is a master regulator of cellular growth. While it’s a normal protein in healthy cells, MYC becomes a malevolent force in cancer, driving uncontrolled tumor growth. Unlike other cancer-causing factors, MYC doesn’t always require a mutation to wreak havoc. Rather, cells produce it relentlessly, making it a hallmark of fast-growing cancers.
“Everyone knows how vital MYC is for cancer, but there are no drugs to block it,” said Joanna Kovalski, PhD, first author of the study. “So, we instead looked toward how MYC is actually made.”
The RBM42 Connection
Using CRISPRi, a cutting-edge gene-editing tool, Kovalski and her team hunted for factors influencing MYC production. Their search led them to RBM42, a protein previously overlooked in cancer research. Analyzing genomic data from pancreatic cancer patients, they found that high levels of RBM42 correlated with elevated MYC and poorer patient outcomes.
When the researchers disrupted RBM42 in pancreatic cancer cells, the results were striking. while MYC mRNA—the blueprint for the protein—was still produced,the cells stopped making MYC protein. This discovery pinpointed RBM42’s role in the translation process, where mRNA is converted into protein.
Hijacking the Protein Assembly Line
Further experiments revealed how RBM42 operates. It reshapes MYC mRNA, making it more efficient for ribosomes—the cell’s protein factories—to process. RBM42 also directs these mRNAs to ribosomes, ensuring MYC is produced in abundance.
“Proteins like RBM42 and MYC exist in every cell but are normally restrained,” explained Davide Ruggero, PhD, senior author of the study. “During cancer, we saw that RBM42 behaved quite differently, hijacking the ribosomes to work with these specific mRNAs and do the cancer’s bidding.”
A Potential Game-Changer
The team tested their approach in both petri dishes and mice. In both cases, removing RBM42 stopped MYC production and halted tumor growth. “RBM42 really seems to be the Achilles’ heel for some of the worst cancers,” Ruggero said.
The researchers beleive small molecules could be developed to disrupt RBM42’s function, effectively jamming cancer’s gears. ”Translation control deserves to be front and centre in our efforts to treat cancer,” Kovalski emphasized. ”We now have grate footing to interfere with the fastest-growing cancers and make a difference for patients.”
Key Insights at a Glance
| Key Finding | Implication |
|————————————–|———————————————————————————|
| RBM42 controls MYC protein production | targeting RBM42 could halt MYC-driven cancers |
| High RBM42 correlates with poor outcomes | RBM42 levels could serve as a prognostic marker for aggressive cancers |
| Disrupting RBM42 stops tumor growth | Potential for developing drugs to block RBM42 and MYC in multiple cancer types |
This discovery opens a new frontier in cancer treatment, offering hope for patients with some of the deadliest forms of the disease. by targeting the machinery behind MYC production, researchers may finally have a way to outsmart cancer’s most resilient driver.
Breaking the MYC code: A new Hope for Halting Cancer’s Deadliest Driver
For decades, scientists have waged war against cancer by targeting mutated proteins in tumors. Yet,many cancers persist,finding ways to outmaneuver these efforts. Now, researchers at UC San Francisco have uncovered a groundbreaking strategy to tackle one of cancer’s most notorious culprits: the MYC protein. Their findings, published in Nature cell Biology, reveal how disrupting a lesser-known protein, RBM42, can effectively halt MYC production, offering a potential lifeline for patients with aggressive cancers.In this interview, Senior Editor of world-today-news.com, Sarah Bennett, speaks with dr. Joanna Kovalski, a leading researcher on the study, to delve into the implications of this discovery.
The MYC Enigma
Sarah Bennett: Dr. Kovalski, thank you for joining us. To start,can you explain why MYC has been such a challenging target in cancer research?
Dr. Kovalski: Absolutely, Sarah. MYC is a master regulator of cellular growth, first identified in the 1970s by UCSF Nobel Laureates Michael Bishop and Harold Varmus. Unlike other cancer-causing factors, MYC doesn’t always require a mutation to wreak havoc. In cancer, cells produce it relentlessly, driving uncontrolled tumor growth. The challenge has been developing drugs to block MYC directly, as it’s deeply embedded in the cell’s regulatory machinery.that’s why we shifted our focus to understanding how MYC is produced in the first place.
the RBM42 Connection
Sarah Bennett: Your team discovered the role of RBM42 in MYC production. Can you walk us through how you identified this connection?
Dr. Kovalski: Sure. We used CRISPRi, a cutting-edge gene-editing tool, to hunt for factors influencing MYC production. This led us to RBM42, a protein previously overlooked in cancer research. When we analyzed genomic data from pancreatic cancer patients, we found that high levels of RBM42 correlated with elevated MYC and poorer patient outcomes. Disrupting RBM42 in pancreatic cancer cells stopped MYC protein production, even though the mRNA blueprint was still present. This revealed RBM42’s critical role in the translation process, where mRNA is converted into protein.
Hijacking the Protein Assembly Line
Sarah Bennett: How exactly does RBM42 facilitate MYC production?
Dr. kovalski: RBM42 reshapes MYC mRNA, making it more efficient for ribosomes—the cell’s protein factories—to process. It also directs these mRNAs to ribosomes, ensuring MYC is produced in abundance. In healthy cells, proteins like RBM42 and MYC are tightly regulated.But in cancer,RBM42 hijacks the ribosomes,forcing them to prioritize MYC production,fueling tumor growth.
A Potential Game-Changer
Sarah Bennett: What are the implications of this discovery for cancer treatment?
Dr. Kovalski: This is a potential game-changer. In our experiments, removing RBM42 stopped MYC production and halted tumor growth in both petri dishes and mice. We believe small molecules could be developed to disrupt RBM42’s function, effectively jamming cancer’s gears. Translation control—how cells convert mRNA into protein—should be front and center in our efforts to treat cancer. By targeting RBM42,we now have a way to interfere with some of the fastest-growing cancers and make a difference for patients.
Key Insights at a Glance
| Key Finding | Implication |
|---|---|
| RBM42 controls MYC protein production | Targeting RBM42 could halt MYC-driven cancers |
| High RBM42 correlates with poor outcomes | RBM42 levels could serve as a prognostic marker for aggressive cancers |
| Disrupting RBM42 stops tumor growth | Potential for developing drugs to block RBM42 and MYC in multiple cancer types |
Conclusion
This discovery opens a new frontier in cancer treatment, offering hope for patients with some of the deadliest forms of the disease. By targeting the machinery behind MYC production, researchers may finally have a way to outsmart cancer’s most resilient driver. Dr.Kovalski’s work underscores the importance of rethinking traditional approaches to cancer therapy and highlights the promise of focusing on the translation process to develop groundbreaking treatments.
