F11r, also known as Junctional Adhesion Molecule -A (JAM -A), is a transmembrane protein belonging to the immunoglobulin superfamily of cell adhesion molecules. It is present in epithelial cells, endothelial cells, leukocytes, and blood platelets. In epithelial and endothelial cells, it is involved in tight junction formation, which is crucial for maintaining cellular layer integrity and selective permeability. In leukocytes, it plays a role in their transmigration through the vascular wall. In platelets, it may regulate downstream signaling of αIIbβ3 integrin [1].

Genetically engineered mice lacking F11r in blood platelets have shown that the protein acts as a negative regulator of a key mechanism triggering platelet aggregation, as these platelets were abnormally reactive [1]. In pancreatic cancer, knocking down F11r in the PANC -1 cell line led to decreased cell proliferation, loss of cell invasiveness, cell cycle arrest in the G1 phase, and enhanced cell apoptosis, suggesting it could be a therapeutic target [2].

In summary, F11r is essential for multiple biological processes such as tight junction formation, leukocyte transmigration, and platelet function. Studies using gene-knockout models, like in platelets and pancreatic cancer cells, have revealed its role in regulating platelet aggregation and pancreatic cancer cell behavior, providing insights into its potential as a therapeutic target in thrombosis-related diseases and pancreatic cancer.

References:

1. Kamola, Piotr, Babinska, Anna, Przygodzki, Tomasz. . F11R/JAM-A: why do platelets express a molecule which is also present in tight junctions? In Platelets, 34, 2214618. doi:10.1080/09537104.2023.2214618. https://pubmed.ncbi.nlm.nih.gov/37246517/

2. Zhang, HaiDi, Zhang, RenDan, Yao, Jiaxin, Mu, Bo, Zhao, ChunYan. 2022. Effect of F11R Gene Knockdown on Malignant Biological Behaviors of Pancreatic Cancer Cells. In Journal of oncology, 2022, 3379027. doi:10.1155/2022/3379027. https://pubmed.ncbi.nlm.nih.gov/35295710/