Sharh maqola

Roles of Non-coding RNAs and Angiogenesis in Glioblastoma

Ebrahim BalandehDepartment of Clinical Psychology, School of Medicine, Kashan University of Medical Sciences, Kashan, IranKimia MohammadshafieDepartment of Biology, Faculty of Science, Golestan University, Gorgan, IranYaser MahmoudiDepartment of Anatomical Sciences, Yasuj University of Medical Sciences, Yasuj, IranMohammad Hossein PourhanifehRazi Drug Research Center, Iran University of Medical Sciences, Tehran, IranAli RajabiSchool of Medicine, Kashan University of Medical Sciences, Kashan, IranZahra Razaghi BahabadiRazi Drug Research Center, Iran University of Medical Sciences, Tehran, IranAmir Hossein MohammadiResearch Center for Biochemistry and Nutrition in Metabolic Diseases, Institute for Basic Sciences, Kashan University of Medical Sciences, Kashan, IranNeda RahimianEndocrine Research Center, Institute of Endocrinology and Metabolism, Iran University of Medical Sciences, Tehran, IranMichael R. HamblinLaser Research Centre, Faculty of Health Science, University of Johannesburg, Doornfontein, South AfricaHamed MirzaeiResearch Center for Biochemistry and Nutrition in Metabolic Diseases, Institute for Basic Sciences, Kashan University of Medical Sciences, Kashan, Iran

2021en

ABI

Annotatsiya

One of the significant hallmarks of cancer is angiogenesis. It has a crucial function in tumor development and metastasis. Thus, angiogenesis has become one of the most exciting targets for drug development in cancer treatment. Here we discuss the regulatory effects on angiogenesis in glioblastoma (GBM) of non-coding RNAs (ncRNAs), including long ncRNA (lncRNA), microRNA (miRNA), and circular RNA (circRNA). These ncRNAs may function in trans or cis forms and modify gene transcription by various mechanisms, including epigenetics. NcRNAs may also serve as crucial regulators of angiogenesis-inducing molecules. These molecules include, metalloproteinases, cytokines, several growth factors (platelet-derived growth factor, vascular endothelial growth factor, fibroblast growth factor, hypoxia-inducible factor-1, and epidermal growth factor), phosphoinositide 3-kinase, mitogen-activated protein kinase, and transforming growth factor signaling pathways.

Hali tarjima qilinmagan

Identifikatorlar

DOI: 10.3389/fcell.2021.716462

Iqtiboslar va manbalar

4 ta iqtibos0 ta foydalanilgan manba

Koʻrsatkichlar — AkademScholar