scholarly journals Roles of Non-coding RNAs and Angiogenesis in Glioblastoma

2021 ◽  
Vol 9 ◽  
Author(s):  
Ebrahim Balandeh ◽  
Kimia Mohammadshafie ◽  
Yaser Mahmoudi ◽  
Mohammad Hossein Pourhanifeh ◽  
Ali Rajabi ◽  
...  
Keyword(s):  
Growth Factor ◽  
Transforming Growth Factor ◽  
Hypoxia Inducible Factor ◽  
Tumor Development ◽  
Circular Rna ◽  
Mitogen Activated Protein Kinase ◽  
Growth Factor Signaling ◽  
Mitogen Activated Protein ◽  
Non Coding Rnas ◽  
Regulatory Effects

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.

scholarly journals Toward Regulatory Effects of Curcumin on Transforming Growth Factor-Beta Across Different Diseases: A Review

2020 ◽  
Vol 11 ◽  
Author(s):  
Milad Ashrafizadeh ◽  
Ali Zarrabi ◽  
Kiavash Hushmandi ◽  
Vahideh Zarrin ◽  
Ebrahim Rahmani Moghadam ◽  
...  
Keyword(s):  
Growth Factor ◽  
Signaling Pathway ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Mitogen Activated Protein Kinase ◽  
Molecular Signaling ◽  
Cellular Events ◽  
Mitogen Activated Protein ◽  
Regulatory Effects

Immune response, proliferation, migration and angiogenesis are juts a few of cellular events that are regulated by transforming growth factor-β (TGF-β) in cells. A number of studies have documented that TGF-β undergoes abnormal expression in different diseases, e.g., diabetes, cancer, fibrosis, asthma, arthritis, among others. This has led to great fascination into this signaling pathway and developing agents with modulatory impact on TGF-β. Curcumin, a natural-based compound, is obtained from rhizome and roots of turmeric plant. It has a number of pharmacological activities including antioxidant, anti-inflammatory, anti-tumor, anti-diabetes and so on. Noteworthy, it has been demonstrated that curcumin affects different molecular signaling pathways such as Wnt/β-catenin, Nrf2, AMPK, mitogen-activated protein kinase and so on. In the present review, we evaluate the potential of curcumin in regulation of TGF-β signaling pathway to corelate it with therapeutic impacts of curcumin. By modulation of TGF-β (both upregulation and down-regulation), curcumin ameliorates fibrosis, neurological disorders, liver disease, diabetes and asthma. Besides, curcumin targets TGF-β signaling pathway which is capable of suppressing proliferation of tumor cells and invading cancer cells.

scholarly journals Specific Activation of Mitogen-activated Protein Kinase by Transforming Growth Factor-β Receptors in Lipid Rafts Is Required for Epithelial Cell Plasticity

2009 ◽  
Vol 20 (3) ◽  
pp. 1020-1029 ◽  
Author(s):  
Wei Zuo ◽  
Ye-Guang Chen
Keyword(s):  
Cell Migration ◽  
Growth Factor ◽  
Protein Kinase ◽  
Lipid Rafts ◽  
Transforming Growth Factor ◽  
Mitogen Activated Protein Kinase ◽  
Type I ◽  
Coated Pits ◽  
Mapk Activation ◽  
Mitogen Activated Protein

Transforming growth factor (TGF)-β regulates a spectrum of cellular events, including cell proliferation, differentiation, and migration. In addition to the canonical Smad pathway, TGF-β can also activate mitogen-activated protein kinase (MAPK), phosphatidylinositol 3-kinase (PI3K)/Akt, and small GTPases in a cell-specific manner. Here, we report that cholesterol depletion interfered with TGF-β–induced epithelial-mesenchymal transition (EMT) and cell migration. This interference is due to impaired activation of MAPK mediated by cholesterol-rich lipid rafts. Cholesterol-depleting agents specifically inhibited TGF-β–induced activation of extracellular signal-regulated kinase (ERK) and p38, but not Smad2/3 or Akt. Activation of ERK or p38 is required for both TGF-β–induced EMT and cell migration, whereas PI3K/Akt is necessary only for TGF-β–promoted cell migration but not for EMT. Although receptor heterocomplexes could be formed in both lipid raft and nonraft membrane compartments in response to TGF-β, receptor localization in lipid rafts, but not in clathrin-coated pits, is important for TGF-β–induced MAPK activation. Requirement of lipid rafts for MAPK activation was further confirmed by specific targeting of the intracellular domain of TGF-β type I receptor to different membrane locations. Together, our findings establish a novel link between cholesterol and EMT and cell migration, that is, cholesterol-rich lipid rafts are required for TGF-β–mediated MAPK activation, an event necessary for TGF-β–directed epithelial plasticity.

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