F11, also known as the F11 Receptor (F11R) or Junctional Adhesion Molecule-A (JAM-A), is a transmembrane glycoprotein of the immunoglobulin superfamily. It is mainly located in epithelial and endothelial cell tight junctions and expressed on circulating platelets and leukocytes. F11R/JAM-A participates in regulating multiple biological processes such as paracellular permeability, tight junction formation and maintenance, leukocyte transendothelial migration, epithelial-to-mesenchymal transition, angiogenesis, reovirus binding, and platelet activation [1]. Dysregulation of F11R/JAM-A may lead to pathological consequences and disorders in normal cell function.

A growing body of evidence indicates its role in carcinogenesis and invasiveness, but its tissue-specific pro-or anti-tumorigenic role remains debated. Understanding the signaling pathways activated or suppressed via the F11R/JAM-A protein in various cancer types is crucial for comprehending its multiple roles in cancer progression and potentially using it as a novel direct target for cancer treatment [1]. Additionally, F11 gene duplication causes elevated FXI plasma levels and is a risk for venous thrombosis [2].

In conclusion, F11 is a significant gene involved in various biological processes, with its dysregulation linked to disease conditions. Research on F11, especially in the context of its role in cancer and thrombosis, has the potential to uncover new therapeutic targets and improve our understanding of these diseases.

References:

1. Czubak-Prowizor, Kamila, Babinska, Anna, Swiatkowska, Maria. 2021. The F11 Receptor (F11R)/Junctional Adhesion Molecule-A (JAM-A) (F11R/JAM-A) in cancer progression. In Molecular and cellular biochemistry, 477, 79-98. doi:10.1007/s11010-021-04259-2. https://pubmed.ncbi.nlm.nih.gov/34533648/

2. Van Laer, Christine, Peerlinck, Kathelijne, Jacquemin, Marc, Labarque, Veerle, Freson, Kathleen. 2021. F11 Gene Duplication Causes Elevated FXI Plasma Levels and Is a Risk for Venous Thrombosis. In Thrombosis and haemostasis, 122, 1058-1060. doi:10.1055/s-0041-1739363. https://pubmed.ncbi.nlm.nih.gov/34781376/