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انتشار مقاله سال 2018
تعداد صفحات مقاله انگلیسی 14 صفحه
هزینه دانلود مقاله انگلیسی رایگان میباشد.
منتشر شده در نشریه هینداوی
نوع مقاله ISI
عنوان انگلیسی مقاله Melatonin Inhibits Reactive Oxygen Species-Driven Proliferation, Epithelial-Mesenchymal Transition, and Vasculogenic Mimicry in Oral Cancer
ترجمه عنوان مقاله جلوگیری ملاتونین از دوباره فعال سازی تکثیر گونه های اکسیژن فعال، انتقال اپیتلیال-مزانشیمال در سرطان دهان
فرمت مقاله انگلیسی  PDF
رشته های مرتبط پزشکی
گرایش های مرتبط غدد و متابولیسم، خون و آنکولوژی
مجله پزشکی اکسیداتیو و طول عمر سلولی – Oxidative Medicine and Cellular Longevity
دانشگاه Department of Stomatology – Third Military Medical University – China
شناسه دیجیتال – doi
https://doi.org/10.1155/2018/3510970
کد محصول E8288
وضعیت ترجمه مقاله  ترجمه آماده این مقاله موجود نمیباشد. میتوانید از طریق دکمه پایین سفارش دهید.
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بخشی از متن مقاله:
1. Introduction

Oral cancer is one of the most common malignancies worldwide [1]. Oral squamous cell carcinoma is the most prevalent type and accounts for 90% of oral cancers [2]. Despite great advances in surgical treatment, radiotherapy, and chemotherapy, the high reoccurrence and poor prognosis of oral cancer appear frequently owing to the rapid growth, local invasiveness, and distant metastasis [3–5]. Thus, exploring the underlying mechanisms of oral cancer growth and metastasis and identifying a potential therapeutic agent for oral cancer are imperative. Reactive oxygen species (ROS) are highly associated with several pathological conditions, including cancers [6]. It is established that cancer cells usually generate a large amount of ROS [7]. ROS can activate Akt signaling responsible for the proliferation and apoptosis evasion in several cancers, including oral cancer [8, 9]. ROS are highly involved in cancer metastasis, which are proposed to be putative mediators or modulators of epithelial-mesenchymal transition (EMT) [10–12]. EMT plays important roles in cancer metastasis and mainly endows cancer cells with invasive phenotypes [13]. During EMT, epithelial cells lose their epithelial markers, such as E-cadherin, and gain the mesenchymal markers, including Vimentin and Snail [14]. Reportedly, Snail is a transcriptional repressor of E-cadherin in tumor cells [15]. Mechanistically, the activation of phosphatidylinositide 3- kinases (PI3K)/Akt pathway is essential for ROS-driven EMT in colon cancer cells; in detail, ROS-dependent Akt activation enhances the expression of Snail and Vimentin and simultaneously reduces E-cadherin expression [16]. ROS is also a critical regulator of angiogenesis that is essential for cancer metastasis [17, 18]. ROS induces the expression of hypoxia-inducible factor 1α (HIF-1α) and increases its stabilization, thereby leading to the upregulation of vascular endothelial growth factor (VEGF) and subsequent angiogenesis [19, 20]. Both extracellular-regulated protein kinases (ERK) and PI3K/Akt pathways greatly contribute to the ROS-enhanced HIF-1α and VEGF during the malignant transformation of human bronchial epithelial cells [21]. Thus, targeting ROS is a potential therapeutic strategy to reduce the malignant phenotypes of oral cancer. Melatonin (N-acetyl-5-methoxytryptamine), which is mainly produced and secreted by the pineal gland, was initially found to be involved in the regulation of chronobiological rhythm [22]. Recently, as a potent antioxidant, melatonin scavenges a variety of free radicals directly and stimulates the activities of antioxidative enzymes indirectly [23, 24]. Melatonin exerts suppressive effects on multiple types of tumors partly depending on free radical scavenging and antioxidative activities [25–27]. Previously, melatonin was utilized as a preventive and curative agent for oral cancers by abolishing oxidative stress [28, 29]. Nevertheless, whether melatonin hampers oral cancer by reducing ROS-increased proliferation, EMT, and angiogenesis remains unknown.

نوشته مقاله انگلیسی رایگان در مورد جلوگیری ملاتونین از فعال سازی تکثیر گونه اکسیژن فعال – هینداوی 2018 اولین بار در سایت آی اس آی دانلود ISIDL. پدیدار شد.

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