Meta-inflammation Increases the Migration and Invasiveness Potential of Prostate Cancer Cells: Investigating the Role of Plectin-1 and S100A4

Authors: Parinita Datta, Zulema Cabail

SUNY Campus: SUNY Old Westbury

Presentation Type: Poster

Location: Old Union Hall

Presentation #: 51

Timeslot: Session D 3:00-4:00 PM

Abstract: Obesity-induced chronic low-grade systemic inflammation, or meta-inflammation, is marked by immune cell accumulation, primarily macrophages, in adipose tissue (AT) and dysregulation of AT hormones and cytokines. Studies suggest obesity increases the risk of fatal prostate cancer (PCa), a leading cause of cancer-related deaths in American men due to its metastatic nature. Within the tumor microenvironment, inflammatory chemokines and cytokines contribute to cancer progression, with macrophages playing a key role in tumorigenesis and metastasis. However, the mechanisms linking obesity and PCa remain unclear. This study investigates the molecular and cellular mechanisms underlying meta-inflammation’s role in PCa migration and invasiveness. Our preliminary data indicate that a hypercaloric environment promotes PCa cell migration and invasion. We hypothesize that this process is regulated by Plectin-1 and S100A4. To test this, U937 human macrophage-like cells were exposed to a lipid-rich microenvironment mimicking obesity-induced inflammation. After 16–18 hours of stimulation with 300 µM sodium palmitate, we collected conditioned media to stimulate DU145 human prostate cancer cells. Invasive behavior was assessed using transwell migration, Boyden chamber invasion, and wound healing assays. Lysates were generated, and protein levels of Plectin-1 and S100A4 will be analyzed via western blotting and immunohistochemistry. Understanding the role of obesity-driven inflammation in PCa progression may provide insights into novel therapeutic targets for metastatic disease.