(source : ANI) ( Photo Credit : ani)
Scientists at UCLA’s Jonsson Comprehensive Cancer Center have uncovered a key player in how leukemia cells thrive: a protein called IGF2BP3. This protein acts like a master switch, connecting the way cancer cells process energy—known as metabolism—with how they tweak their own genetic instructions through RNA regulation.
Leukemia cells constantly push to grow and spread, often by revamping their metabolism to grab quick energy from sugar and altering RNA to build the proteins they need to survive. IGF2BP3 ties these two survival tricks together. It pushes cells toward glycolysis, a fast but wasteful way to break down sugar that gives cancer the building blocks for rapid multiplication. At the same time, it modifies RNA to boost protein production essential for leukemia’s aggressive spread.
“We knew IGF2BP3 could handle RNA, but we didn’t expect it to reshape metabolism so dramatically,” said Dr. Dinesh Rao, a professor of pathology and laboratory medicine at UCLA’s David Geffen School of Medicine and the study’s senior author. “This link is new and could explain how leukemia cells get their edge. By targeting it, we might disrupt both their energy supply and survival signals.”
Rao’s team has tracked IGF2BP3 for nearly a decade. Normally, this RNA-binding protein works only in early human development and quiets down after birth. But in cancers like leukemia, brain tumors, sarcomas, and breast cancer, it reactivates and becomes crucial for cell survival. Their past work showed it’s vital for an aggressive form of pediatric acute lymphoblastic leukemia—mice without the protein resisted the disease but stayed healthy otherwise.
To dig deeper, the researchers used a tool called the Seahorse assay, which tracks how cells breathe oxygen and produce acid, basically testing their energy-burning efficiency like a workout monitor. Without IGF2BP3, leukemia cells sharply cut back on glycolysis. Further tests revealed dropping levels of SAM, a molecule that adds chemical tags to RNA. This drop reduced RNA methylation marks, proving IGF2BP3 not only controls genes but also loops back to tweak metabolism for better RNA control.
In mouse experiments, removing the IGF2BP3 gene halted these changes, but adding back the human version restored the metabolic and RNA shifts, locking in the protein’s central role.
“It’s a chain reaction,” explained Dr. Gunjan Sharma, a postdoctoral scholar in Rao’s lab. “Knocking out IGF2BP3 didn’t just alter energy use—it threw off the cells’ chemical balance and RNA regulation. That’s how we saw it links metabolism and RNA control in leukemia.”
The discovery shows IGF2BP3 doesn’t just chase efficiency; it favors this sloppy metabolic path because it provides raw materials and RNA tweaks that supercharge cancer survival. “IGF2BP3 is like a master planner,” Sharma added. “It rewires energy and RNA to let leukemia cells grow where normal ones wouldn’t.”
Though focused on leukemia, the findings could apply to many cancers. “We’re seeing this clearly in leukemia, but other cancer cells likely use the same playbook,” Rao said. He’s part of UCLA’s Jonsson Cancer Center and the Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research. High IGF2BP3 levels might even serve as a biomarker to spot cancers responsive to drugs targeting RNA modifications or SAM production.
Rao’s lab now tests small molecules to block IGF2BP3, aiming to pair them with metabolism-disrupting drugs for stronger leukemia treatments and beyond. This breakthrough in cancer research opens doors to smarter therapies that hit leukemia cells where it hurts.
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