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Researchers at Fox Chase Cancer Center have pinpointed a protein called ANO6 as a promising new target in pancreatic cancer. In preclinical studies, blocking ANO6 slowed tumor growth and helped immune cells fight back more effectively. The findings, published in Nature Cancer, could open a new front in one of oncology's toughest battles.
Pancreatic cancer is notoriously hard to treat, partly because tumors are surrounded by dense tissue that shields them from both drugs and the immune system. Now, Fox Chase Cancer Center researchers may have found a key vulnerability: a protein called anoctamin 6 (ANO6), with findings published in Nature Cancer.
ANO6 sits on cancer-associated fibroblasts (CAFs) — cells that make up much of the dense tissue around pancreatic tumors. The researchers discovered that CAFs use a process called trogocytosis to ferry cholesterol and other lipids directly to cancer cells, fueling their growth. ANO6 is the gatekeeper of this transfer. The same cholesterol handoff also exhausts cancer-fighting T cells, giving tumors a double advantage. When the team blocked ANO6 — using existing drugs niclosamide and clofazimine — tumors in mouse models shrank significantly, and T cells regained their cancer-killing activity.
Key Takeaways:
Why it matters: Pancreatic ductal adenocarcinoma has a 5-year survival rate of under 15%. A target that disrupts both nutrient supply and immune evasion simultaneously could represent a meaningful step toward more effective therapies.
