کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10899391 | 1084371 | 2016 | 12 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Astemizole-Histamine induces Beclin-1-independent autophagy by targeting p53-dependent crosstalk between autophagy and apoptosis
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کلمات کلیدی
b2mUNC-51-like kinasepoly (ADP-ribose) polymerase 1GRP-78N-acetyl-l-cysteinesequestosome 1DRAMBH3H1RCCAAT/enhancer-binding protein (C/EBP) homologous proteinHprtUPRATGPKCp62LC3eIF2αRAPAMPKEMSAJnkautophagy proteinPARP-1p53TSC5' AMP-activated protein kinaseprotein kinase R-like endoplasmic reticulum kinaseNACmTORATFBcl-2damage-regulated autophagy modulatorc-Jun N-terminal kinases - C-Jun N-terminal kinasescAMP - cAMPH2DCFDA - H2DCFD بهIRE1α - IRE1aMAPK - MAPKROS - ROSCyclic adenosine monophosphate - آدنوزین مونوفسفات CyclicElectrophoretic mobility shift assay - آزمون تحرک تحرک الکتروفورزAST - آسپارتات ترانس آمینازinositol-requiring enzyme 1 - آنزیم مورد نیاز inositol 1Astemizole - استامیزولER stress - استرس استBeta-2-microglobulin - بتا-2-میکروگلوبولینTerminal deoxynucleotidyl transferase dUTP nick end labeling - ترمینال deoxynucleotidyl transferase dUTP نام نهایی پایان نامهTUNEL - تونلCHOP - تکه کردنApoptosis - خزان یاختهایHIS - خودRapamycin - راپامایسینendoplasmic reticulum - شبکه آندوپلاسمی activating transcription factor - فعال کردن عامل رونویسیB cell lymphoma 2 - لنفوم سلول B 2mammalian target of rapamycin - هدف پستانداران رپامایسینHistamine - هیستامینhypoxanthine-guanine phosphoribosyltransferase - هیپوکسانتین-گوانین فسفریبوسیل ترانسفرازUnfolded protein response - پاسخ پروتئین آشکارglucose-regulated protein 78 - پروتئین تنظیم شده با گلوکز 78Protein kinase C - پروتئین کیناز سیPERK - پرکBID - پیشنهادTuberous sclerosis complex - کمپلکس توبروس اسکلروزیسmitogen-activated protein kinases - کیناز پروتئین فعال MitogenReactive oxygen species - گونههای فعال اکسیژنH1 receptor - گیرنده H1histamine H1 receptor - گیرنده هیستامین H1
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
تحقیقات سرطان
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Apoptosis and autophagy are genetically regulated, evolutionarily conserved processes that can jointly seal cancer cell fates, and numerous death stimuli are capable of activating either pathway. Although crosstalk between apoptosis and autophagy is quite complex and sometimes contradictory, it remains a key factor determining the outcomes of death-related pathologies such as cancer. In the present study, exposure of MCF-7 breast cancer cells to HIS and the H1 receptor antagonist AST both alone and together with HIS (AST-HIS) led to generation of intracellular ROS, which induced massive cellular vacuolization through dilation of the ER and mitochondria. Consequently, apoptosis by Bax translocation, cytochrome c release, and caspase activation were triggered. In addition, AST-HIS caused ER stress-induced autophagy in MCF-7 cells, as evidenced by an increased LC3-II/LC3-I ratio, with surprisingly no changes in Beclin-1 expression. Non-canonical autophagy was induced via p53 phosphorylation, which increased p53-p62 interactions to enhance Beclin-1-independent autophagy as evidenced by immunocytochemistry and immunoprecipitation. In the absence of Beclin-1, enhanced autophagy further activated apoptosis through caspase induction. In conclusion, these findings indicate that AST-HIS-induced apoptosis and autophagy can be regulated by ROS-mediated signaling pathways.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Cancer Letters - Volume 372, Issue 1, 1 March 2016, Pages 89-100
Journal: Cancer Letters - Volume 372, Issue 1, 1 March 2016, Pages 89-100
نویسندگان
Rekha Jakhar, Souren Paul, Monika Bhardwaj, Sun Chul Kang,