Biomolecules Involved in Both Metastasis and Placenta Accreta Spectrum—Does the Common Pathophysiological Pathway Exist?

SIMPLE SUMMARY: Both invasive placentation and cancer metastasis involve the intricate migration and invasion of cells into the surrounding tissues, while also creating new blood vessels to support their growth. The complex interplay of molecular signals that regulate cell behavior, including growth factors, cytokines, and extracellular matrix components, plays a crucial role in both processes. Despite their differing physiological contexts and evolutionary origins, invasive placentation and cancer metastasis share many molecular and cellular mechanisms that allow them to invade and proliferate in the surrounding tissues. In both pathological conditions, cells need to overcome the local mechanisms of immunological defense, activate invasion, and induce angiogenesis. This article focuses on describing the biomolecules that link these pathological processes. ABSTRACT: The process of epithelial-to-mesenchymal transition (EMT) is crucial in the implantation of the blastocyst and subsequent placental development. The trophoblast, consisting of villous and extravillous zones, plays different roles in these processes. Pathological states, such as placenta accreta spectrum (PAS), can arise due to dysfunction of the trophoblast or defective decidualization, leading to maternal and fetal morbidity and mortality. Studies have drawn parallels between placentation and carcinogenesis, with both processes involving EMT and the establishment of a microenvironment that facilitates invasion and infiltration. This article presents a review of molecular biomarkers involved in both the microenvironment of tumors and placental cells, including placental growth factor (PlGF), vascular endothelial growth factor (VEGF), E-cadherin (CDH1), laminin γ2 (LAMC2), the zinc finger E-box-binding homeobox (ZEB) proteins, αVβ3 integrin, transforming growth factor β (TGF-β), β-catenin, cofilin-1 (CFL-1), and interleukin-35 (IL-35). Understanding the similarities and differences in these processes may provide insights into the development of therapeutic options for both PAS and metastatic cancer.