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Angioregulatory role of miRNAs and exosomal miRNAs in glioblastoma pathogenesis.
Bouzari, B, Mohammadi, S, Bokov, DO, Krasnyuk, II, Hosseini-Fard, SR, Hajibaba, M, Mirzaei, R, Karampoor, S
Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie. 2022;:112760
Abstract
Glioblastoma (GB) is a highly aggressive cancer of the central nervous system, occurring in the brain or spinal cord. Many factors such as angiogenesis are associated with GB development. Angiogenesis is a procedure by which the pre-existing blood vessels create new vessels that play an essential role in health and disease, including tumors. Also, angiogenesis is one of the significant factors thought to be responsible for treatment resistance in many tumors, including GB. Hence, an improved understanding of the molecular processes underlying GB angiogenesis will pave the way for developing potential new treatments. Recently, it has been found that microRNAs (miRNAs) and exosomal miRNAs have a crucial role in inducing or inhibiting the angiogenesis process in GB development. A better knowledge of the miRNA's regulation pathway in the angiogenesis process in cancer offers unique mechanistic insight into the mechanism of tumor-associated neovascularization. Because of advancements in miRNA characterization and delivery methods, miRNAs can also be employed in clinical settings as potential biomarkers for anti-angiogenic treatment response as well as therapies targeting tumor angiogenesis. The recent finding and insights about miRNAs' angioregulatory role and exosomal miRNAs in GB are provided throughout the review. Also, we discuss the new concept of miRNAs-based therapies for GB in the future.
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Future Perspectives of Therapeutic, Diagnostic and Prognostic Aptamers in Eye Pathological Angiogenesis.
Iturriaga-Goyon, E, Buentello-Volante, B, Magaña-Guerrero, FS, Garfias, Y
Cells. 2021;(6)
Abstract
Aptamers are single-stranded DNA or RNA oligonucleotides that are currently used in clinical trials due to their selectivity and specificity to bind small molecules such as proteins, peptides, viral particles, vitamins, metal ions and even whole cells. Aptamers are highly specific to their targets, they are smaller than antibodies and fragment antibodies, they can be easily conjugated to multiple surfaces and ions and controllable post-production modifications can be performed. Aptamers have been therapeutically used for age-related macular degeneration, cancer, thrombosis and inflammatory diseases. The aim of this review is to highlight the therapeutic, diagnostic and prognostic possibilities associated with aptamers, focusing on eye pathological angiogenesis.
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3.
Tumor angiogenesis: Current challenges and therapeutic opportunities.
Al-Ostoot, FH, Salah, S, Khamees, HA, Khanum, SA
Cancer treatment and research communications. 2021;:100422
Abstract
Angiogenesis plays an important role in the development of cancer since it allows for the delivery of oxygen, nutrients, and growth factors as well as tumor dissemination to distant organs. Inhibition of angiogenesis is an important strategy for the prevention of multiple solid tumors that depend on cutting or at least reducing the blood supply to tumor micro-regions, resulting in pan-hypoxia and pan-necrosis within solid tumor tissues. These drugs are an important part of treatment for some types of cancer. As a stand-alone therapy, inhibition of tumor angiogenesis can arrest or halt tumor growth, but will not eliminate the tumor. Therefore, anti-angiogenic drugs in combinations with another anti-cancer treatment method, like chemotherapy, lead to being critical for optimum cancer patient outcomes. Over the last two decades, investigations have been made to improve the efficacy of anti-angiogenic drugs, recognize their potential in drug interactions, and come up with plausible explanations for possible treatment resistance. This review will offer an overview of the varying concepts of tumor angiogenesis, several important angiogenic factors; focus on the role of anti-angiogenesis strategies in cancer treatment.
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4.
Role of small interfering RNA (siRNA) in targeting ocular neovascularization: A review.
Supe, S, Upadhya, A, Singh, K
Experimental eye research. 2021;:108329
Abstract
Ocular neovascularization (NV) plays a central role in the pathogenesis of various ocular diseases including diabetic retinopathy, age-related macular degeneration, retinoblastoma, retinitis pigmentosa and may lead to loss of vision if not controlled in time. Several clinical trials elucidate the central role of vascular endothelial growth factor (VEGF) in the pathogenesis of the ocular neovascularization. The advent and extensive use of ocular anti-VEGF therapy heralded a new age in the treatment of retinal vascular and exudative diseases. RNA interference (RNAi) can be used to inhibit the in-vitro and in-vivo expression of specific genes and thus provides an extremely useful method for investigating gene activity with minimal toxicity. siRNA targeting VEGF overcomes many drawbacks associated with the conventional treatment available for the treatment of ocular neovascularization. However, delivery methods that protect the siRNA against degradation and are appropriate for long-term care will help increase the effectiveness of RNAi-based anti-VEGF ocular therapies. Several nanotechnology approaches have been explored by formulation scientists for delivery of siRNA to the eye; targeting particularly VEGF for the treatment of NV. This review mainly focuses on current updates in various pre-clinical and clinical siRNA strategies for targeting VEGF involved in the development of ocular neovascularization.
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Mechanisms of lncRNA/microRNA interactions in angiogenesis.
Zhao, Z, Sun, W, Guo, Z, Zhang, J, Yu, H, Liu, B
Life sciences. 2020;:116900
Abstract
Angiogenesis is a complex physiological process. However, over the past couple of decades, abnormally accelerated or pathological angiogenesis has garnered greater attention from researchers the world over. Studies have shown that this abnormal and uncontrolled angiogenesis not only promotes inflammatory responses but also plays a role in various malignant and cardiovascular diseases. These include solid tumors, atherosclerosis, blinding retinopathy, and other diseases. Furthermore, there is mounting evidence that noncoding RNAs, especially lncRNAs and microRNAs, play important roles in the regulation of angiogenesis. In recent years, numerous studies have found that lncRNA may serve as an endogenous sponge to regulate the expression and function of miRNA, which in turn bind to lncRNA, regulating their stability. Therefore, this review focuses on the mechanisms of lncRNA/microRNA interactions in angiogenesis. A better understanding of such lncRNA/microRNA interactions may provide helpful insights and shed new light on areas of research for identifying diagnostic markers and therapeutic approaches for treating angiogenesis-related diseases.
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6.
Parallels of Resistance between Angiogenesis and Lymphangiogenesis Inhibition in Cancer Therapy.
Jones, D
Cells. 2020;(3)
Abstract
Metastasis is the primary cause of cancer-related mortality. Cancer cells primarily metastasize via blood and lymphatic vessels to colonize lymph nodes and distant organs, leading to worse prognosis. Thus, strategies to limit blood and lymphatic spread of cancer have been a focal point of cancer research for several decades. Resistance to FDA-approved anti-angiogenic therapies designed to limit blood vessel growth has emerged as a significant clinical challenge. However, there are no FDA-approved drugs that target tumor lymphangiogenesis, despite the consequences of metastasis through the lymphatic system. This review highlights several of the key resistance mechanisms to anti-angiogenic therapy and potential challenges facing anti-lymphangiogenic therapy. Blood and lymphatic vessels are more than just conduits for nutrient, fluid, and cancer cell transport. Recent studies have elucidated how these vasculatures often regulate immune responses. Vessels that are abnormal or compromised by tumor cells can lead to immunosuppression. Therapies designed to improve lymphatic vessel function while limiting metastasis may represent a viable approach to enhance immunotherapy and limit cancer progression.
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Vascular endothelial growth factor: An important molecular target of curcumin.
Saberi-Karimian, M, Katsiki, N, Caraglia, M, Boccellino, M, Majeed, M, Sahebkar, A
Critical reviews in food science and nutrition. 2019;(2):299-312
Abstract
The discovery of Vascular Endothelial Growth Factor (VEGF), the key modulator of angiogenesis, has triggered intensive research on anti-angiogenic therapeutic modalities. Although several clinical studies have validated anti-VEGF therapeutics, with few of them approved by the U.S. Food and Drug Administration (FDA), anti-angiogenic therapy is still in its infancy. Phytochemicals are compounds that have several metabolic and health benefits. Curcumin, the yellow pigment derived from turmeric (Curcuma longa L.) rhizomes, has a wide range of pharmaceutical properties. It has also been shown to inhibit VEGF by several studies. In this review, we elaborate the effect of curcumin on VEGF and angiogenesis and its therapeutic application.
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Potential molecular mechanisms underlying the effect of arsenic on angiogenesis.
Zhang, J, Zhang, Y, Wang, W, Zhang, Z
Archives of pharmacal research. 2019;(11):962-976
Abstract
Arsenic is a potent chemotherapeutic drug that is applied as a treatment for cancer; it exerts its functions through multiple pathways, including angiogenesis inhibition. As angiogenesis is a critical component of the progression of many diseases, arsenic is a feasible treatment option for patients with other angiogenic diseases, including rheumatoid arthritis and psoriasis, among others. However, arsenic is also a well-known carcinogen, demonstrating a pro-angiogenesis effect. This review will focus on the dual effects of arsenic on neovascularization and the relevant mechanisms underlying these effects, aiming to provide a rational understanding of arsenic treatment. In particular, we expect to provide a comprehensive overview of the current knowledge of the mechanisms by which arsenic influences angiogenesis.
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Annexin A2 (ANX A2): An emerging biomarker and potential therapeutic target for aggressive cancers.
Sharma, MC
International journal of cancer. 2019;(9):2074-2081
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Abstract
ANX A2 is an important member of annexin family of proteins expressed on surface of endothelial cells (ECs), macrophages, mononuclear cells and various types of cancer cells. It exhibits high affinity binding for calcium (Ca++ ) and phospholipids. ANX A2 plays an important role in many biological processes such as endocytosis, exocytosis, autophagy, cell-cell communications and biochemical activation of plasminogen. On the cell surface ANX A2 organizes the assembly of plasminogen (PLG) and tissue plasminogen activator (tPA) for efficient conversion of PLG to plasmin, a serine protease. Proteolytic activity of plasmin is required for activation of inactive pro-metalloproteases (pro-MMPs) and latent growth factors for their biological actions. These activation steps are critical for degradation of extracellular matrix (ECM) and basement proteins (BM) for cancer cell invasion and metastasis. Increased expression of ANX A2 protein/gene has been correlated with invasion and metastasis in a variety of human cancers. Moreover, clinical studies have positively correlated ANX A2 protein expression with aggressive cancers and with resistance to anticancer drugs, shorter disease-free survival (DFS), and worse overall survival (OS). The mechanism(s) by which ANX A2 regulates cancer invasion and metastasis are beginning to emerge. Investigators used various technologies to target ANX A2 in preclinical model of human cancers and demonstrated exciting results. In this review article, we analyzed existing literature concurrent with our own findings and provided a critical overview of ANX A2-dependent mechanism(s) of cancer invasion and metastasis.
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Multiple modes of action of eribulin mesylate: Emerging data and clinical implications.
Cortes, J, Schöffski, P, Littlefield, BA
Cancer treatment reviews. 2018;:190-198
Abstract
Eribulin mesylate (eribulin) is a synthetic analogue of the marine-sponge natural product halichondrin B. Eribulin exhibits potent antiproliferative activities against a variety of human cancer cell types in vitro and in vivo, and is used for the treatment of certain patients with advanced breast cancer or liposarcoma who are refractory to other treatments. The antiproliferative effects of eribulin have long been attributed to its antimitotic activities. Unlike other microtubule-targeting agents, eribulin inhibits microtubule polymerization through specific plus end binding, thus interfering with microtubule dynamic instability. Non-mitotic effects of eribulin on tumor biology have also been established in laboratory settings including: tumor vasculature remodeling, increased vascular perfusion, reduced hypoxia, and phenotypic changes involving reversal of epithelial-to-mesenchymal transition (EMT), resulting in reduced capacities for migration, invasion, and seeding lung metastases in experimental models. Preclinical data suggest that increased perfusion following eribulin treatment improves delivery of subsequent drugs. Supporting evidence for eribulin's non-mitotic effects in the clinical setting include increased tumor oxygen saturation, reduced hypoxia, phenotype changes consistent with EMT reversal, and genotype changes consistent with shifts from nonendocrine-responsive, luminal B, to endocrine-responsive, luminal A, breast cancer subtypes. Finally, potential biomarkers for eribulin response have been established based on tumor-phenotype and gene-expression profiles. Overall, preclinical and clinical data support both antimitotic and non-mitotic mechanisms of eribulin that may underlie the survival benefit observed in various clinical trials.