Pancreatic cancer is one of the most aggressive and deadly forms of cancer, with only about 10% of patients surviving more than five years after diagnosis.
One reason it’s so hard to treat is the tumor’s surrounding environment, called the stroma.
This dense layer, which makes up most of the tumor, is filled with support cells and proteins that actually help the cancer grow and resist treatment.
Among the most important of these support cells are fibroblasts, which help cancer cells survive and spread.
Now, a groundbreaking international study has found a surprising new way these fibroblasts promote pancreatic cancer—through a protein called Galectin-1.
Researchers from the Hospital del Mar Research Institute in Spain, Mayo Clinic, the Instituto de Biología y Medicina Experimental in Argentina, and the CaixaResearch Institute have discovered that Galectin-1 doesn’t just work outside of cells, as previously thought.
It also plays a powerful role inside the nuclei of fibroblasts, where it influences how certain genes are turned on or off.
Their findings were recently published in the journal PNAS.
Dr. Pilar Navarro, the lead researcher, explained that the stroma protects cancer cells and creates a barrier that limits how well treatments like chemotherapy can work.
Fibroblasts are a major part of this system, and they release substances—like Galectin-1—that help tumors grow.
But this new research shows that Galectin-1 isn’t just secreted outside cells. It also acts from inside the cell nucleus, where it controls the activity of key genes without changing the DNA itself. This process is known as epigenetic regulation.
One of the genes affected by Galectin-1 is KRAS, which is mutated in around 90% of pancreatic cancer cases. KRAS is a major driver of cancer growth and aggressiveness. The fact that Galectin-1 can influence KRAS activity inside fibroblasts makes it a key player in helping tumors grow.
Previously, scientists have tried to block the effects of Galectin-1 outside the fibroblasts to slow tumor growth. But this study shows that those efforts may not be enough.
According to Dr. Neus Martínez-Bosch, who also worked on the study, future treatments need to target Galectin-1 inside the fibroblasts too, especially in the cell nucleus where it plays this newly discovered role.
To uncover these findings, the research team studied tissue samples from pancreatic cancer patients and conducted lab experiments with human fibroblast cells. When they blocked Galectin-1 and the KRAS gene in these cells, the fibroblasts became inactive and stopped helping the tumor grow.
Dr. Judith Vinaixa, the study’s first author, said this work confirms that Galectin-1 is essential for controlling genes that determine how fibroblasts behave.
Dr. Gabriel Rabinovich, one of the collaborating scientists, added that targeting Galectin-1—both inside and outside cells—could become a powerful way to fight pancreatic cancer. Because the protein also supports blood vessel formation and blocks immune system attacks, stopping it could make many cancer treatments work better.
These discoveries could lead to new and more effective treatments for one of the world’s deadliest cancers.
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Source: KSR.
