Even with recent progress,
cancer remains the second leading cause of death, outlining a need to widen the current understanding on oncogenic factors. Accumulating evidence from recent years suggest
Contactin 1 (CNTN1)'s possession of multiple oncogenic activities in a variety of
cancer types. CNTN1 is a
cell adhesion molecule that is dysregulated in many human
carcinomas and plays important roles in
cancer progression and
metastases. Abnormalities in CNTN1 expression associate with
cancer progression and poor prognosis. Mechanistically, CNTN1 functions in various signaling pathways frequently altered in
cancer, such as the
vascular endothelial growth factor C (VEGFC)-
VEGF receptor 3 (VEFGR3)/fms-related
tyrosine kinase 4 (Flt4) axis,
phosphatidylinositol 3-kinase (PI3K)/
protein kinase B (AKT), Notch signaling pathway and epithelial-mesenchymal transition (EMT) process. These oncogenic events are resulted via interactions between
tumor and stroma, which can be contributed by CNTN1, an adhesion
protein. CNTN1 expression in
breast cancer correlates with the expression of genes functioning in
cancer-stroma interactions and skeletal system development. Evidence supports that CNTN1 promotes
cancer-stromal interaction, resulting in activation of a complex network required for
cancer progression and
metastasis (bone
metastasis for
breast cancer). CNTN1 inhibitions has been proven to be effective in experimental models to reduce
oncogenesis. In this paper, we will review CNTN1's alterations in
cancer, its main biochemical mechanisms and interactions with its relevant
cancer pathways.