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학술저널
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You, Zhi-Mei (Laboratory of Stem Cells and Tissue Engineering, Department of Histology and Embryology, Chongqing Medical University) Zhao, Liang (Laboratory of Stem Cells and Tissue Engineering, Department of Histology and Embryology, Chongqing Medical University) Xia, Jing (Laboratory of Stem Cells and Tissue Engineering, Department of Histology and Embryology, Chongqing Medical University) Wei, Qiang (Laboratory of Stem Cells and Tissue Engineering, Department of Histology and Embryology, Chongqing Medical University) Liu, Yu-Min (College of Pharmacy, the First Affiliated Hospital, Chongqing Medical University) Liu, Xiao-Yan (Department of Geriatrics, the First Affiliated Hospital, Chongqing Medical University) Chen, Di-Long (Laboratory of Stem Cells and Tissue Engineering, Department of Histology and Embryology, Chongqing Medical University) Li, Jing (Laboratory of Stem Cells and Tissue Engineering, Department of Histology and Embryology, Chongqing Medical University)
저널정보
아시아태평양암예방학회 Asian Pacific journal of cancer prevention : APJCP Asian Pacific journal of cancer prevention : APJCP 제15권 제3호
발행연도
2014.1
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1,099 - 1,104 (6page)

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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 are significant, the underlying mechanisms remain unknown. In this study, we sought to elucidate possible links between ginsenoside Rh2 and phosphoglucose isomerase/autocrine motility factor (PGI/AMF). Methods: $KG1{\alpha}$, 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 and flow cytometry (FCM) were adopted to investigate the effects of Rh2 on PGI/AMF. The relationships between PGI/AMF and Rh2 associated with Akt, mTOR, Raptor, Rag were detected by western blot analysis. Results: KG1${\alpha}$ cells expressed PGI/AMF and its down-regulation significantly inhibited proliferation. The antibody array indicated that the probable mechanism was reduced expression of PARP, State1, SAPK/JNK and Erk1/2, while those of PRAS40 and p38 were up-regulated. Silencing of PGI/AMF enhanced the sensibility of $KG1{\alpha}$ to Rh2 by suppressing the expression of mTOR, Raptor and Akt. Conclusion: These results suggested that ginsenoside Rh2 suppressed the proliferation of $KG1{\alpha}$, the same as down-regulation of PGI/AMF. Down-regulation of PGI/AMF enhanced the pharmacological effects of ginsenoside Rh2 on KG1${\alpha}$ by reducing Akt/mTOR signaling.

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