Unexpected Role of Cancer-Related Gene in Pancreatic Tumor Growth

Recent research from Indiana University School of Medicine has uncovered a surprising function of a well-known cancer-fighting gene within the tumor microenvironment, specifically in pancreatic cancer. The study, published in Science Advances, focused on M2-like macrophages—immune cells that can support tumor growth when altered. Scientists investigated the gene, serine/threonine kinase 11 (STK11), historically recognized as a tumor suppressor, and discovered it plays a crucial role in regulating macrophage behavior. When STK11 is absent in these immune cells, they switch to a tumor-supporting state, thereby aiding cancer progression.

In mouse models of pancreatic cancer, the loss of STK11 in macrophages was linked to accelerated tumor development. This finding reveals an unexpected role of STK11 in shaping immune cell function within tumors, beyond its known effects on directly controlling cancer cell growth. As Dr. Kai Yang explained, "Instead of directly acting on tumors, STK11 in macrophages helps prevent these cells from aiding cancer. When the gene is missing, macrophages may support tumor growth instead."

The implications of this discovery suggest that enhancing STK11 activity or interfering with pathways that promote macrophage tumor support could improve treatment strategies for pancreatic and other cancers. Future research will aim to understand how STK11 influences the tumor immune environment as cancer advances, potentially unveiling new therapeutic targets.

Additional co-authors include Jing Yang, Naresh Singh, Chengxian Xu, and others from Indiana University. This new insight into immune cell regulation underscores the complexity of tumor microenvironments and opens avenues for innovative immunotherapies.

Source: Medical Xpress