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1.
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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2.
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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5.
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.
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7.
Connective tissue growth factor (CTGF) in age-related vascular pathologies.
Ungvari, Z, Valcarcel-Ares, MN, Tarantini, S, Yabluchanskiy, A, Fülöp, GA, Kiss, T, Csiszar, A
GeroScience. 2017;(5-6):491-498
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Abstract
Connective tissue growth factor (CTGF, also known as CCN2) is a matricellular protein expressed in the vascular wall, which regulates diverse cellular functions including cell adhesion, matrix production, structural remodeling, angiogenesis, and cell proliferation and differentiation. CTGF is principally regulated at the level of transcription and is induced by mechanical stresses and a number of cytokines and growth factors, including TGFβ. In this mini-review, the role of age-related dysregulation of CTGF signaling and its role in a range of macro- and microvascular pathologies, including pathogenesis of aorta aneurysms, atherogenesis, and diabetic retinopathy, are discussed. A potential role of CTGF and TGFβ in regulation and non-cell autonomous propagation of cellular senescence is also discussed.
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Angiopoietin 2 in placentation and tumor biology: The yin and yang of vascular biology.
Wang, Q, Lash, GE
Placenta. 2017;:73-78
Abstract
There are several parallels between placental and tumor biology. Both require rapid acquisition of a blood supply to supply oxygen and nutrients, the placenta through neoangiogenesis and tumors by co-opting the existing vasculature. In addition, successful pregnancy also requires remodeling of the maternal uterine spiral arteries. Angiopoietins (Angs) are a family of angiogenic growth factors, the best studied being Ang-1 and Ang-2, which signal through the membrane tyrosine kinase receptor Tie2, and in simple terms have opposite effects with Ang-1 acting to stabilize newly formed blood vessels and Ang-2 having a destabilizing effect. The roles of Ang-1, and in particular Ang-2 in placental and tumor biology are discussed in this review.
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Neurovascular cross talk in diabetic retinopathy: Pathophysiological roles and therapeutic implications.
Moran, EP, Wang, Z, Chen, J, Sapieha, P, Smith, LE, Ma, JX
American journal of physiology. Heart and circulatory physiology. 2016;(3):H738-49
Abstract
Diabetic retinopathy (DR) is the leading cause of blindness in the working-age population in developed countries, and its prevalence will increase as the global incidence of diabetes grows exponentially. DR begins with an early nonproliferative stage in which retinal blood vessels and neurons degenerate as a consequence of chronic hyperglycemia, resulting in vasoregression and persistent retinal ischemia, metabolic disequilibrium, and inflammation. This is conducive to overcompensatory pathological neovascularization associated with advanced proliferative DR. Although DR is considered a microvascular complication, the retinal microvasculature is intimately associated with and governed by neurons and glia; neurodegeneration, neuroinflammation, and dysregulation of neurovascular cross talk are responsible in part for vascular abnormalities in both early nonproliferative DR and advanced proliferative DR. Neuronal activity directly regulates microvascular dilation and blood flow in the process of neurovascular coupling. Retinal neurons also secrete guidance cues in response to injury, ischemia, or metabolic stress that may either promote or suppress vascular outgrowth, either alleviating or exacerbating DR, contingent on the stage of disease and retinal microenvironment. Neurodegeneration, impaired neurovascular coupling, and dysregulation of neuronal guidance cues are key events in the pathogenesis of DR, and correcting these events may prevent or delay development of advanced DR. The review discusses the mechanisms of neurovascular cross talk and its dysregulation in DR, and their potential therapeutic implications.
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10.
Targeting of proangiogenic signalling pathways in chronic inflammation.
Tas, SW, Maracle, CX, Balogh, E, Szekanecz, Z
Nature reviews. Rheumatology. 2016;(2):111-22
Abstract
Angiogenesis is de novo capillary outgrowth from pre-existing blood vessels. This process not only is crucial for normal development, but also has an important role in supplying oxygen and nutrients to inflamed tissues, as well as in facilitating the migration of inflammatory cells to the synovium in rheumatoid arthritis, spondyloarthritis and other systemic autoimmune diseases. Neovascularization is dependent on the balance of proangiogenic and antiangiogenic mediators, including growth factors, cytokines, chemokines, cell adhesion molecules and matrix metalloproteinases. This Review describes the various intracellular signalling pathways that govern these angiogenic processes and discusses potential approaches to interfere with pathological angiogenesis, and thereby ameliorate inflammatory disease, by targeting these pathways.