Szczegóły publikacji

Cancer cell migration is a key step in the metastatic cascade. Understanding its mechanisms represents one of the greatest challenges in modern oncology. Both in vitro and in vivo experimental models and mathematical descriptions of movement dynamics are used to study this complex phenomenon. These models allow for the quantitative characterization of movement trajectories based on cell motion parameters. Within the tumor microenvironment, the human cathelicidin LL-37 holds a special place as a regulator of these processes. This article summarizes current knowledge (until July 2025) on LL-37’s involvement in cancer cell migration across several cancer types. LL-37 has been implicated in tumor progression through modulation of signaling pathways, epithelial-mesenchymal transition, and angiogenesis, highlighting it as a potential target for research into mechanisms of cancer invasion and metastasis. LL-37 serves as an agonist of multiple receptors, initiating signaling pathways. Its effects are highly dependent on the tumor type, receptor expression, concentration, and exposure time. Data show that in most studied epithelial tumors, including breast, hepatocellular, and squamous cell carcinomas, LL-37 typically promotes cell migration and invasiveness. However, in glioma and colon cancer (being a notable epithelial exception) this peptide inhibits motility. Understanding mechanisms of LL-37 action opens new perspectives in the search for therapeutic strategies aimed at controlling the invasiveness and metastatic potential of tumor cells. At the same time, the more widespread use of mathematical models in medicine creates the prospect of developing effective therapies that inhibit the ability of cancers to metastasize.