کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10899718 | 1084401 | 2015 | 9 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Hypoxia-induced IL-32β increases glycolysis in breast cancer cells
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کلمات کلیدی
LDH-APDK1HIF-1PPPOXPHOSOCRIL-32ECARPP2APKM2ROS - ROSInterleukin-32 - اینترلوکین 32Mitochondrial biogenesis - زیست زیستی میتوکندریاییhypoxia inducible factor-1 - عامل القایی هیپوکسی 1Oxidative phosphorylation - فسفوریلاسیون اکسیداتیوLactate dehydrogenase A - لاکتات دهیدروژناز Apentose phosphate pathway - مسیر پنتوز فسفاتOxygen consumption rate - میزان مصرف اکسیژنextracellular acidification rate - نرخ اسیدی شدن خارج سلولیHypoxia - هیپوکسیprotein phosphatase 2A - پروتئین فسفاتاز 2APyruvate kinase M2 - پیروات کیناز M2Pyruvate dehydrogenase kinase - پیرووات دهیدروژناز کینازGlycolysis - گلیکولیز یا قندکافتReactive oxygen species - گونههای فعال اکسیژن
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
تحقیقات سرطان
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
IL-32β is highly expressed and increases the migration and invasion of gastric, lung, and breast cancer cells. Since IL-32 enhances VEGF production under hypoxic conditions, whether IL-32β is regulated by hypoxia was examined. Hypoxic conditions and a mimetic chemical CoCl2 enhanced IL-32β production. When cells were treated with various inhibitors of ROS generation to prevent hypoxia-induced ROS function, IL-32β production was suppressed by both NADPH oxidase and mitochondrial ROS inhibitors. IL-32β translocated to the mitochondria under hypoxic conditions, where it was associated with mitochondrial biogenesis. Thus, whether hypoxia-induced IL-32β is associated with oxidative phosphorylation (OXPHOS) or glycolysis was examined. Glycolysis under aerobic and anaerobic conditions is impaired in IL-32β-depleted cells, and the hypoxia-induced IL-32β increased glycolysis through activation of lactate dehydrogenase. Src is also known to increase lactate dehydrogenase activity, and the hypoxia-induced IL-32β was found to stimulate Src activation by inhibiting the dephosphorylation of Src. These findings revealed that a hypoxia-ROS-IL-32β-Src-glycolysis pathway is associated with the regulation of cancer cell metabolism.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Cancer Letters - Volume 356, Issue 2, Part B, 28 January 2015, Pages 800-808
Journal: Cancer Letters - Volume 356, Issue 2, Part B, 28 January 2015, Pages 800-808
نویسندگان
Jeong Su Park, Sunyi Lee, Ae Lee Jeong, Sora Han, Hye In Ka, Jong-Seok Lim, Myung Sok Lee, Do-Young Yoon, Jeong-Hyung Lee, Young Yang,