Pancreatic cancer is one of the most dangerous types of cancer, with a survival rate of just 10% after five years. One reason it is so difficult to treat is because of its tumor microenvironment, or stroma, which makes up most of the tumor’s mass.
This stroma is not made of cancer cells but is a complex network of proteins and other cell types that help the tumor survive and grow. A key part of this environment is fibroblasts—supportive cells that, unfortunately, assist cancer cells in resisting treatment and spreading.
Now, a team of international scientists has discovered a surprising new function of a protein called Galectin-1, which could explain why pancreatic tumors are so aggressive and hard to treat.
The study, recently published in the journal PNAS, was led by researchers from the Hospital del Mar Research Institute in Spain, along with partners from Mayo Clinic, Argentina’s CONICET, and the CaixaResearch Institute.
Galectin-1 is already known to be a pro-tumor protein. Previously, researchers believed that fibroblasts helped tumors by releasing Galectin-1 into the area surrounding the tumor, where it supported cancer growth. But this new study shows that Galectin-1 doesn’t just act outside the fibroblasts—it also plays a crucial role inside their nuclei.
Dr. Pilar Navarro, the senior researcher of the project, explained that Galectin-1 inside fibroblasts actually changes the way these cells behave by altering gene activity. Specifically, it affects gene expression without changing the DNA code itself—a process known as epigenetic regulation.
One of the key genes it influences is KRAS, which is a major driver of pancreatic cancer and is mutated in around 90% of patients.
This discovery is important because it reveals a hidden layer of how pancreatic cancer resists treatment. If Galectin-1 inside fibroblast nuclei can turn these cells into active supporters of the tumor, then current strategies that only target the protein outside the cell may not be enough.
The researchers used tissue samples from pancreatic cancer patients and also conducted experiments in the lab with human fibroblast cell lines. By blocking Galectin-1 or turning off the KRAS gene in these cells, they were able to stop the fibroblasts from helping the cancer grow.
This showed that both Galectin-1 and KRAS are key parts of the machinery that turns ordinary cells into cancer allies.
Dr. Neus Martínez-Bosch, another researcher on the team, emphasized that this changes the direction of future treatment efforts. “Until now, most efforts have been focused on stopping Galectin-1 in the tumor’s surroundings,” she said. “But now we know we also need to block its activity inside fibroblasts.”
Dr. Judith Vinaixa, the study’s first author, highlighted that this internal role of Galectin-1 helps control many genes important to how fibroblasts behave. Meanwhile, Dr. Gabriel Rabinovich, another lead researcher, said the next step is to find treatments that can block both the inside and outside actions of Galectin-1.
This dual approach could be even more effective, especially since the protein is also involved in helping tumors build blood vessels and resist immunotherapy.
This new understanding opens the door to better, more targeted treatments for pancreatic cancer. Instead of only attacking cancer cells, future therapies may also target the cells that support tumors from the inside out.
If scientists can find ways to stop Galectin-1 both outside and inside fibroblasts, it may be possible to weaken the tumor’s defenses and improve survival for one of the deadliest cancers.
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The research findings can be found in PNAS.
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