فایل ورد (word) مقاله Down-regulation of Phosphoglucose Isomerase/Autocrine Motility Factor Enhances Gensenoside Rh2 Pharmacological Action on Leukemia KG1? Cells دارای 10 صفحه می باشد و دارای تنظیمات در microsoft word می باشد و آماده پرینت یا چاپ است
فایل ورد فایل ورد (word) مقاله Down-regulation of Phosphoglucose Isomerase/Autocrine Motility Factor Enhances Gensenoside Rh2 Pharmacological Action on Leukemia KG1? Cells کاملا فرمت بندی و تنظیم شده در استاندارد دانشگاه و مراکز دولتی می باشد.
توجه : در صورت مشاهده بهم ريختگي احتمالي در متون زير ،دليل ان کپي کردن اين مطالب از داخل فایل ورد مي باشد و در فايل اصلي فایل ورد (word) مقاله Down-regulation of Phosphoglucose Isomerase/Autocrine Motility Factor Enhances Gensenoside Rh2 Pharmacological Action on Leukemia KG1? Cells،به هيچ وجه بهم ريختگي وجود ندارد
بخشی از متن فایل ورد (word) مقاله Down-regulation of Phosphoglucose Isomerase/Autocrine Motility Factor Enhances Gensenoside Rh2 Pharmacological Action on Leukemia KG1? Cells :
سال انتشار : 2014
تعداد صفحات :10
Aims and Background: Ginsenoside Rh2, which exerts the potent anticancer action both in vitro and in vivo,is one of the most well characterized ginsenosides extracted from ginseng. Although its effects on cancer aresignificant, the underlying mechanisms remain unknown. In this study, we sought to elucidate possible linksbetween ginsenoside Rh2 and phosphoglucose isomerase/autocrine motility factor (PGI/AMF). Methods: KG1,a leukemia cell line highly expressing PGI/AMF was assessed by western blot analysis and reverse transcription-PCR (RT-PCR) assay after transfection of a small interfering (si)-RNA to silence PGI/AMF. The effect of PGI/AMF on proliferation was measured by typan blue assay and antibody array. A cell counting kit (CCK)-8 andflow cytometry (FCM) were adopted to investigate the effects of Rh2 on PGI/AMF. The relationships betweenPGI/AMF and Rh2 associated with Akt, mTOR, Raptor, Rag were detected by western blot analysis. Results:KG1 cells expressed PGI/AMF and its down-regulation significantly inhibited proliferation. The antibody arrayindicated that the probable mechanism was reduced expression of PARP, State1, SAPK/JNK and Erk1/2, whilethose of PRAS40 and p38 were up-regulated. Silencing of PGI/AMF enhanced the sensibility of KG1 to Rh2by suppressing the expression of mTOR, Raptor and Akt. Conclusion: These results suggested that ginsenosideRh2 suppressed the proliferation of KG1, the same as down-regulation of PGI/AMF. Down-regulation of PGI/AMF enhanced the pharmacological effects of ginsenoside Rh2 on KG1 by reducing Akt/mTOR signaling.