Figure 2.

Interaction between ovarian cancer (OC) cells and adipose tissue (AT) within the tumor microenvironment (TME). The microenvironment within the peritoneal cavity is crucial for OC pathogenesis. The close collaboration between cancer cells, stromal cells, and adipocytes produces outcomes that flow in both directions. The stroma and AT play a vital role as a pre-metastatic niche, while cancer cells disrupt the normal adipose and stromal tissue, adapting it to their needs and creating an environment more conducive to cancer growth. Pro-inflammatory macrophages form a ring around dying and necrotic adipocytes (CAA—cancer-associated adipocytes), forming a crown-like structure (CLS). The development of cancer cells in the peritoneum tends to occur in the omental milky spots, lymphoid structures found in the omentum. CA125 and the overexpression of MMPs promote the adhesion of cancer cells into the peritoneal mesothelial layer. Afterward, the close interaction between CAA in the omentum and cancer cells stimulates tumor proliferation by various mechanisms: boosting a vast extracellular matrix (ECM), inducing a senescent-like phenotype, exchanging metabolites, and promoting immune regulation.