Abstract
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.
Highlights
Cell adhesion molecules (CAMs) are membrane receptors that bind to extracellular matrix molecules or receptors [1]
Contactin 1 (CNTN1) expression was elevated in multidrug resistance (MDR) A549/cisplatin (A549/DDP) cells compared to its progenitor A549 lung cancer cells, and the silencing of CNTN1 rendered both cells higher cisplatin sensitivity and upregulated cisplatin-induced apoptosis, leading to inhibition of tumor invasion and metastasis [59]
In the concept of “molecular targeted therapy”, correcting for alterations that occur in cancer progression and metastasis remains the fundamental goal
Summary
Cell adhesion molecules (CAMs) are membrane receptors that bind to extracellular matrix molecules or receptors [1]. CAMs play important rolescause in regulating thesepatients homotypic and interactions [1,2,4] This well-orchestrated process follows few key including is tumour cell invasion of the primary site, intravasation into blood and/or. Despite beingorprimarily studied for its roles in thewhich human nervous system, CNTN1 has been interactions with extracellular matrix (ECM) in the tumour microenvironment. (GPI)-anchored neural cell adhesion molecules of the immunoglobulin poor prognosis phosphatidylinositol [6,7] On these premises, the interest of CNTN1 as a target to impede cancer progression superfamily (IgSF) [5]. The aberrant activation s involvement of CNTN1 has been reported to be involved in pathological phenotypes such as cell proliferation, in cancer progression and metastasis, and its related molecular mechanisms. Reviewed [6,8], and some findings have been made and will be discussed
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
