کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8292546 | 1536733 | 2018 | 7 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
JLP-JNK signaling protects cancer cells from reactive oxygen species-induced cell death
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کلمات کلیدی
shRNAJBDJLPc-Jun NH2-terminal kinasePARPGSTFBSJnkPBSHCC - HCCMAPK - MAPKshort hairpin RNA - RNA موی سر کوتاهROS - ROSHydrogen peroxide - آب اکسیژنهOxidative stress - تنش اکسیداتیوdihydroethidium - دی هیدروتیدیمfetal bovine serum - سرم جنین گاوPhosphate buffered saline - فسفات بافر شورCell death - مرگ سلولی Knockdown - نابودیhemagglutinin - هماگلوتینینH2O2 - هیدروژن پراکسیدDHE - وpolymerase chain reaction - واکنش زنجیره ای پلیمرازPCR - واکنش زنجیرهٔ پلیمرازScaffold protein - پروتئین داربستmitogen-activated protein kinase - پروتئین کیناز فعال با mitogenPropidium iodide - پروتئین یدیدPoly(ADP-ribose) polymerase - پلیمر (ADP-ribose) پلیمرازHepatocellular carcinoma - کارسینوم هپاتوسلولار(کارسینوم سلولهای استخوانی)glutathione S-transferase - گلوتاتیون S-ترانسفرازReactive oxygen species - گونههای فعال اکسیژن
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Oxidative stress, which can be caused by an overproduction of reactive oxygen species (ROS), often leads to cell death. In recent years, c-Jun NH2-terminal kinase (JNK)-associated leucine zipper protein (JLP, also known as SPAG9 or JIP4), a scaffold protein for JNK mitogen-activated protein kinase (MAPK) signaling pathways, was found to serve as a novel biomarker for cancer. However, although JNK MAPK pathways are reported to be activated in response to various stimuli, including oxidative stress, whether JLP is involved in ROS signaling remains unknown. In this study, we examined the role of JLP in hydrogen peroxide (H2O2)-induced cancer cell death, and found that JLP knockdown (KD) cells exhibit a substantially enhanced cell death response, along with increased intracellular ROS levels. This is the first demonstration of a protective role for JLP in response to cell-death stimulation. We also found that the H2O2-induced JNK activation was attenuated in JLP KD cancer cells. The decreases in cell viability and JNK activation in the JLP KD cells were almost completely reversed by expressing wild-type JLP, but not a mutant JLP lacking the JNK-binding domain. These data collectively suggest that the JLP-JNK signaling pathway counteracts ROS-induced cancer cell death.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochemical and Biophysical Research Communications - Volume 501, Issue 3, 27 June 2018, Pages 724-730
Journal: Biochemical and Biophysical Research Communications - Volume 501, Issue 3, 27 June 2018, Pages 724-730
نویسندگان
Rong Li, I. Ketut Gunarta, Ryusuke Suzuki, Jambaldorj Boldbaatar, Ryota Nakazato, Dewi Yuliana, Gantulga Davaakhuu, Tsendsuren Oyunsuren, Nobuhiko Takamatsu, Masahiko Kobayashi, Atsushi Hirao, Katsuji Yoshioka,