Περίληψη:
During development, as tissues expand and grow, they require circulatory, lymphatic, and nervous system expansion for proper function and support. Similarly, as tumors arise and develop, they also require the expansion of these systems to support them. While the contribution of blood and lymphatic systems to the development and progression of cancer is well known and is targeted with anticancer drugs, the contribution of the nervous system is less well studied and understood. Recent studies have shown that the interaction between neurons and a tumor are bilateral and promote metastasis on one hand, and the formation of new nerve structures (neoneurogenesis) on the other. Substances such as neurotransmitters and neurotrophins being the main actors in such interplay, it seems reasonable to expect that alternative splicing and the different populations of protein isoforms can affect tumor-derived neurogenesis. Here, we report the different, documented ways in which neurons contribute to the development and progression of cancer and investigate what is currently known regarding cancer-neuronal interaction in several specific cancer types. Furthermore, we discuss the incidence of alternative splicing that have been identified as playing a role in tumor-induced neoneurogenesis, cancer development and progression. Several examples of changes in alternative splicing that give rise to different isoforms in nerve tissue that support cancer progression, growth and development have also been investigated. Finally, we discuss the potential of our knowledge in alternative splicing to improve tumor diagnosis and treatment. © 2021 by the authors. Licensee MDPI, Basel, Switzerland.
Συγγραφείς:
Dlamini, Z.
Mathabe, K.
Padayachy, L.
Marima, R.
Evangelou, G.
Syrigos, K.N.
Bianchi, A.
Lolas, G.
Hull, R.
Λέξεις-κλειδιά:
acetylcholine; amphiphysin; antisense oligonucleotide; beta 2 adrenergic receptor; beta 3 adrenergic receptor; brain derived neurotrophic factor receptor; catecholamine; cyclic AMP responsive element binding protein; doublecortin; epinephrine; fibroblast growth factor receptor 1; G protein coupled receptor; G protein coupled receptor kinase; G protein coupled receptor kinase interacting protein 1; glial cell line derived neurotrophic factor; histone demethylase; histone demethylase BHC80; isoprotein; mitogen activated protein kinase; monophenol monooxygenase; muscarinic receptor; nerve growth factor; neurotransmitter; neurotrophin; noradrenalin; nusinersen; phosphatidylinositol 3 kinase; RNA; TAR DNA binding protein; unclassified drug; vasculotropin, adrenergic system; alternative RNA splicing; angiogenesis; Article; autonomic nervous system; breast cancer; cancer cell; carcinogenesis; cell interaction; cell stress; cholinergic system; depression; drug targeting; glioblastoma; head and neck cancer; hematologic malignancy; human; intestine innervation; lymphangiogenesis; malignant neoplasm; metastasis potential; nerve cell; nerve cell differentiation; nervous tissue; nonhuman; ovary cancer; pancreas cancer; perineural invasion; prostate cancer; stomach cancer; tumor growth
