Abstract
Neurodevelopmental programs are frequently dysregulated in cancer. Semaphorins are a large family of guidance cues that direct neuronal network formation and are also implicated in cancer. Semaphorins have two kinds of receptors, neuropilins and plexins. Besides their role in development, semaphorin signaling may promote or suppress tumors depending on their context. Sema3C is a secreted semaphorin that plays an important role in the maintenance of cancer stem-like cells, promotes migration and invasion, and may facilitate angiogenesis. Therapeutic strategies that inhibit Sema3C signaling may improve cancer control. This review will summarize the current research on the Sema3C pathway and its potential as a therapeutic target.
Highlights
The connection between neural networks and cancer has long been recognized
More recent data reveal that neural stimulation can trigger a release of neurotransmitters that contribute to the growth, differentiation, and proliferation of tumor cells and cancer stem-like cells (CSCs) [1]
Others have shown that expression of attractive cues from Semaphorin 3C (Sema3C) and PlexinD1 and repulsive cues from Sema3D, Sema6A, Sema6B, and PlexinA1 guide the migration of cardiac neural crest cells [31,32]
Summary
The connection between neural networks and cancer has long been recognized. In almost all solid tumors, perineural invasion is recognized as an important adverse prognostic feature. Many neural developmental programs are hijacked by cancer cells to promote their own growth, survival, and invasion These programs include axonal guidance proteins and their receptors, notably the Eph/ephrin [2], Slit/Robo [3], neurotrophin [4], Netrin/DCC/UNC5 [5,6], and Semaphorin/Neuropilin/Plexin families of proteins [7,8,9,10,11,12,13]. These axonal guidance systems promote cancer growth themselves, and promote migration and angiogenesis. We will introduce the role of Sema3C signaling in development and focus on the role of Sema3C and its receptors in oncogenesis and in CSCs
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