The F11 Receptor (F11R), also called Junctional Adhesion Molecule-A (JAM-A) (F11R/JAM-A), is a transmembrane glycoprotein of the immunoglobulin superfamily, which is mainly located in epithelial and endothelial cell tight junctions and also expressed on circulating platelets and leukocytes. It participates in the regulation of various biological processes, as diverse as paracellular permeability, tight junction formation and maintenance, leukocyte transendothelial migration, epithelial-to-mesenchymal transition, angiogenesis, reovirus binding, and platelet activation. Dysregulation of F11R/JAM-A may result in pathological consequences and disorders in normal cell function. A growing body of evidence points to its role in carcinogenesis and invasiveness, but its tissue-specific pro- or anti-tumorigenic role remains a debated issue. The following review focuses on the F11R/JAM-A tissue-dependent manner in tumorigenesis and metastasis and also discusses the correlation between poor patient clinical outcomes and its aberrant expression. In the future, it will be required to clarify the signaling pathways that are activated or suppressed via the F11R/JAM-A protein in various cancer types to understand its multiple roles in cancer progression and further use it as a novel direct target for cancer treatment.

中文翻译：

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癌症进展中的 F11 受体 (F11R)/连接粘附分子-A (JAM-A) (F11R/JAM-A)。

F11受体（F11R），也称为连接粘附分子-A（JAM-A）（F11R/JAM-A），是免疫球蛋白超家族的一种跨膜糖蛋白，主要位于上皮细胞和内皮细胞紧密连接处，也表达对循环血小板和白细胞。它参与各种生物过程的调节，如细胞旁通透性、紧密连接的形成和维持、白细胞跨内皮迁移、上皮-间质转化、血管生成、呼肠孤病毒结合和血小板活化。F11R/JAM-A 的失调可能导致正常细胞功能的病理后果和紊乱。越来越多的证据表明它在致癌和侵袭中的作用，但其组织特异性促或抗肿瘤作用仍然是一个有争议的问题。以下综述侧重于 F11R/JAM-A 在肿瘤发生和转移中的组织依赖性方式，并讨论了患者临床结果不佳与其异常表达之间的相关性。未来，需要阐明在各种癌症类型中通过 F11R/JAM-A 蛋白激活或抑制的信号通路，以了解其在癌症进展中的多重作用，并进一步将其作为癌症治疗的新直接靶点.