20(S)-ginsenoside Rh2 inhibits the proliferation and induces the apoptosis of KG-1a cells through the Wnt/β-catenin signaling pathway.

Publication Dbxref
PMID:27121661
Title
20(S)-ginsenoside Rh2 inhibits the proliferation and induces the apoptosis of KG-1a cells through the Wnt/β-catenin signaling pathway.
Publication Type
Journal Article
Series Name
Oncology reports
Volume
36
Publication Year
2016
Issue
1
Page Numbers
137-46
DOI
10.3892/or.2016.4774
Journal Abbreviation
Oncol Rep
EISSN
1791-2431
Publication Date
2016 Jul
Citation
Chen Y, Liu ZH, Xia J, Li XP, Li KQ, Xiong W, Li J, Chen DL. 20(S)-ginsenoside Rh2 inhibits the proliferation and induces the apoptosis of KG-1a cells through the Wnt/β-catenin signaling pathway.. Oncology reports. 2016 Jul; 36(1):137-46.
ISSN
1791-2431
Language Abbr
eng
Publication Model
Print-Electronic
Authors
Chen Y, Liu ZH, Xia J, Li XP, Li KQ, Xiong W, Li J, Chen DL
Language
English
Elocation
10.3892/or.2016.4774
Journal Country
Greece
Abstract

Previous research has shown that total saponins of Panax ginseng (TSPG) and other ginsenoside monomers inhibit the proliferation of leukemia cells. However, the effect has not been compared among them. Cell viability was determined by Cell Counting Kit-8 assay, and ultra-structural characteristics were observed under transmission electron microscopy. Cell cycle distribution and apoptosis were determined by flow cytometry (FCM). Real-time fluorescence quantitative‑PCR, western blotting and immunofluorescence were used to measure the expression of β-catenin, TCF4, cyclin D1 and NF-κBp65. β-catenin/TCF4 target gene transcription were observed by ChIP-PCR assay. We found that 20(S)-ginsenoside Rh2 [(S)Rh2] inhibited the proliferation of KG-1a cells more efficiently than the other monomers. Moreover, (S)Rh2 arrested KG-1a cells in the G0/G1 phase and induced apoptosis. In addition, the levels of β-catenin, TCF4, cyclin D1 mRNA and protein were decreased. The ChIP-PCR showed that (S)Rh2 downregulated the transcription of β-catenin/TCF4 target genes, such as cyclin D1 and c-myc. These results indicated that (S)Rh2 induced cell cycle arrest and apoptosis through the Wnt/β-catenin signaling pathway, demonstrating its potential as a chemotherapeutic agent for leukemia therapy.

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