Abstract
Ovarian cancer is the eighth most common cancer in women worldwide, and epithelial ovarian cancer (EOC) represents 90% of cases. Nerve growth factor (NGF) and its high affinity receptor tyrosine kinase A receptor (TRKA) have been associated with the development of several types of cancer, including EOC; both NGF and TRKA levels are elevated in this pathology. EOC presents high angiogenesis and several molecules have been reported to induce this process. NGF increases angiogenesis through its TRKA receptor on endothelial cells, and by indirectly inducing vascular endothelial growth factor expression. Other molecules controlled by NGF include ciclooxigenase-2, disintegrin and metalloproteinase domain-containing protein 17 (ADAM17) and calreticulin (CRT), proteins involved in crucial processes needed for EOC progression. These molecules could be modified through microRNA regulation, which could be regulated by NGF. MicroRNAs are the widest family of non-coding RNAs; they bind to 3′-UTR of mRNAs to inhibit their translation, to deadenilate or to degraded them. In EOC, a deregulation in microRNA expression has been described, including alterations of miR-200 family, cluster-17-92, and miR-23b, among others. Since the NGF-microRNA relationship in pathologies has not been studied, this review proposes that some microRNAs could be associated with NGF/TRKA activation, modifying protein levels needed for EOC progression.
Highlights
Ovarian cancer is a deadly disease that causes over 140,000 deaths every year [1]
Neurotrophins are a family of small polypeptides growth factors that consists of five members: Nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), neurotrophin 3 (NT-3), neurotrophin 4/5 (NT-4/5) and neurotrophin 6 (NT-6) [49]
NGF is able to induce Vascular endothelial growth factor (VEGF) expression through Tyrosine kinase A receptor (TRKA) activation [69]. These findings suggest that NGF and TRKA are important in the regulation of the normal ovarian function
Summary
Ovarian cancer is a deadly disease that causes over 140,000 deaths every year [1]. Nerve growth factor (NGF) and its high affinity receptor, Tyrosine kinase A receptor (TRKA), are overexpressed in ovarian cancer and they have been associated with increased proliferation, survival and angiogenesis [3]. NGF, through TRKA activation, can alter the expression of several molecules associated with cancer development and progression [3]. MiRs are small non-coding RNA molecules that downregulate gene expression by acting on mRNAs [6]. Several miRs have been linked to cancer, either through overexpression or downregulation, altering the levels of oncogenes or tumor suppressor genes [7]. A potential link between EOC, NGF and miRs is established
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