Induction of G1 cell cycle arrest and p27(KIP1) increase by panaxydol isolated from Panax ginseng

Jungae Moon, Su Jin Yu, Hyeon Soo Kim, Jeongwon Sohn

Research output: Contribution to journalArticle

33 Citations (Scopus)

Abstract

Polyacetylenic compounds of Panax ginseng roots have been shown to inhibit growth of several human malignant tumor cell lines. Panaxydol is known to be one of the cytotoxic polyacetylenic compounds of P. ginseng. In this study, we first showed that panaxydol decreased markedly the proliferation, and to a lesser extent, the number of cells in a human melanoma cell line, SK-MEL-1. Next, the effect of panaxydol on cell cycle progression and its mechanism of action were investigated. Cell cycle analysis revealed that panaxydol inhibited cell cycle progression of a human malignant melanoma cell line, SK-MEL-1, at G1-S transition. At the same time, panaxydol increased the protein expression of p27(KIP1) as early as 1 hr after treatment. Cyclin-dependent kinase 2 (Cdk2) activity was decreased in a dose-dependent manner after 24 hr of panaxydol treatment. Protein levels of p21(WAF1), p16(INK4a), p53, pRb (retinoblastoma protein), and E2F-1 were not changed. It was also found that cycloheximide reversed the growth inhibition induced by panaxydol and partially abrogated the increase in p27(KIP1) expression. These results indicate that panaxydol induces G1 cell cycle arrest by decreasing Cdk2 activity and up-regulating p27(KIP1) protein expression. Copyright (C) 2000 Elsevier Science Inc.

Original languageEnglish
Pages (from-to)1109-1116
Number of pages8
JournalBiochemical Pharmacology
Volume59
Issue number9
DOIs
Publication statusPublished - 2000 May 1

Fingerprint

G1 Phase Cell Cycle Checkpoints
Panax
Cells
Cyclin-Dependent Kinase 2
Cell Cycle
Melanoma
Cell Line
Retinoblastoma Protein
Proteins
panaxydol
Cycloheximide
Growth
Tumor Cell Line
Tumors
Cell Count

Keywords

  • Cdk2
  • Cell cycle
  • G arrest
  • Melanoma
  • p27(KIP1)
  • Panaxydol

ASJC Scopus subject areas

  • Pharmacology

Cite this

Induction of G1 cell cycle arrest and p27(KIP1) increase by panaxydol isolated from Panax ginseng. / Moon, Jungae; Yu, Su Jin; Kim, Hyeon Soo; Sohn, Jeongwon.

In: Biochemical Pharmacology, Vol. 59, No. 9, 01.05.2000, p. 1109-1116.

Research output: Contribution to journalArticle

@article{f207e43c16ab4aefb70cfb6eca37b198,
title = "Induction of G1 cell cycle arrest and p27(KIP1) increase by panaxydol isolated from Panax ginseng",
abstract = "Polyacetylenic compounds of Panax ginseng roots have been shown to inhibit growth of several human malignant tumor cell lines. Panaxydol is known to be one of the cytotoxic polyacetylenic compounds of P. ginseng. In this study, we first showed that panaxydol decreased markedly the proliferation, and to a lesser extent, the number of cells in a human melanoma cell line, SK-MEL-1. Next, the effect of panaxydol on cell cycle progression and its mechanism of action were investigated. Cell cycle analysis revealed that panaxydol inhibited cell cycle progression of a human malignant melanoma cell line, SK-MEL-1, at G1-S transition. At the same time, panaxydol increased the protein expression of p27(KIP1) as early as 1 hr after treatment. Cyclin-dependent kinase 2 (Cdk2) activity was decreased in a dose-dependent manner after 24 hr of panaxydol treatment. Protein levels of p21(WAF1), p16(INK4a), p53, pRb (retinoblastoma protein), and E2F-1 were not changed. It was also found that cycloheximide reversed the growth inhibition induced by panaxydol and partially abrogated the increase in p27(KIP1) expression. These results indicate that panaxydol induces G1 cell cycle arrest by decreasing Cdk2 activity and up-regulating p27(KIP1) protein expression. Copyright (C) 2000 Elsevier Science Inc.",
keywords = "Cdk2, Cell cycle, G arrest, Melanoma, p27(KIP1), Panaxydol",
author = "Jungae Moon and Yu, {Su Jin} and Kim, {Hyeon Soo} and Jeongwon Sohn",
year = "2000",
month = "5",
day = "1",
doi = "10.1016/S0006-2952(00)00235-5",
language = "English",
volume = "59",
pages = "1109--1116",
journal = "Biochemical Pharmacology",
issn = "0006-2952",
publisher = "Elsevier Inc.",
number = "9",

}

TY - JOUR

T1 - Induction of G1 cell cycle arrest and p27(KIP1) increase by panaxydol isolated from Panax ginseng

AU - Moon, Jungae

AU - Yu, Su Jin

AU - Kim, Hyeon Soo

AU - Sohn, Jeongwon

PY - 2000/5/1

Y1 - 2000/5/1

N2 - Polyacetylenic compounds of Panax ginseng roots have been shown to inhibit growth of several human malignant tumor cell lines. Panaxydol is known to be one of the cytotoxic polyacetylenic compounds of P. ginseng. In this study, we first showed that panaxydol decreased markedly the proliferation, and to a lesser extent, the number of cells in a human melanoma cell line, SK-MEL-1. Next, the effect of panaxydol on cell cycle progression and its mechanism of action were investigated. Cell cycle analysis revealed that panaxydol inhibited cell cycle progression of a human malignant melanoma cell line, SK-MEL-1, at G1-S transition. At the same time, panaxydol increased the protein expression of p27(KIP1) as early as 1 hr after treatment. Cyclin-dependent kinase 2 (Cdk2) activity was decreased in a dose-dependent manner after 24 hr of panaxydol treatment. Protein levels of p21(WAF1), p16(INK4a), p53, pRb (retinoblastoma protein), and E2F-1 were not changed. It was also found that cycloheximide reversed the growth inhibition induced by panaxydol and partially abrogated the increase in p27(KIP1) expression. These results indicate that panaxydol induces G1 cell cycle arrest by decreasing Cdk2 activity and up-regulating p27(KIP1) protein expression. Copyright (C) 2000 Elsevier Science Inc.

AB - Polyacetylenic compounds of Panax ginseng roots have been shown to inhibit growth of several human malignant tumor cell lines. Panaxydol is known to be one of the cytotoxic polyacetylenic compounds of P. ginseng. In this study, we first showed that panaxydol decreased markedly the proliferation, and to a lesser extent, the number of cells in a human melanoma cell line, SK-MEL-1. Next, the effect of panaxydol on cell cycle progression and its mechanism of action were investigated. Cell cycle analysis revealed that panaxydol inhibited cell cycle progression of a human malignant melanoma cell line, SK-MEL-1, at G1-S transition. At the same time, panaxydol increased the protein expression of p27(KIP1) as early as 1 hr after treatment. Cyclin-dependent kinase 2 (Cdk2) activity was decreased in a dose-dependent manner after 24 hr of panaxydol treatment. Protein levels of p21(WAF1), p16(INK4a), p53, pRb (retinoblastoma protein), and E2F-1 were not changed. It was also found that cycloheximide reversed the growth inhibition induced by panaxydol and partially abrogated the increase in p27(KIP1) expression. These results indicate that panaxydol induces G1 cell cycle arrest by decreasing Cdk2 activity and up-regulating p27(KIP1) protein expression. Copyright (C) 2000 Elsevier Science Inc.

KW - Cdk2

KW - Cell cycle

KW - G arrest

KW - Melanoma

KW - p27(KIP1)

KW - Panaxydol

UR - http://www.scopus.com/inward/record.url?scp=0033963112&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0033963112&partnerID=8YFLogxK

U2 - 10.1016/S0006-2952(00)00235-5

DO - 10.1016/S0006-2952(00)00235-5

M3 - Article

VL - 59

SP - 1109

EP - 1116

JO - Biochemical Pharmacology

JF - Biochemical Pharmacology

SN - 0006-2952

IS - 9

ER -