A recent study from UC San Diego has identified the enzyme MICAL2 as a significant player in pancreatic cancer progression, particularly in pancreatic ductal adenocarcinomas (PDAC). The study reveals that MICAL2 is found in much higher concentrations in PDAC tumor cells than in healthy cells, indicating its role in tumor growth and metastasis. Researchers discovered that patients with low MICAL2 levels in their tumors tend to survive approximately twice as long as those with higher levels, suggesting that the enzyme contributes to advancing the disease.
MICAL2 enhances the activity of the KRAS signaling pathway, which is crucial for regulating cell growth and is the main driver of pancreatic tumor progression. Silencing the MICAL2 gene in cancer cells significantly impairs the KRAS pathway, reducing tumor growth. Given its critical role, MICAL2 presents a potential target for new therapies aimed at addressing the high mortality associated with pancreatic cancer, which currently claims around 50,000 lives annually in the U.S. According to senior author Dr. Andrew Lowy, developing drugs to inhibit MICAL2 could lead to improved treatment options for patients facing this aggressive cancer. The findings are slated for publication on January 2, 2025, in the journal Cancer Research.
