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Mechanisms of 2-methoxyestradiol-induced apoptosis and G2/M cell-cycle arrest of nasopharyngeal carcinoma cells

Abstract 2-Methoxyestradiol (2ME2) is an endogenous metabolite of 17β-estradiol (E2 ). This study aims to examine the anti-tumour activities of 2ME2 on the poorly differentiated HONE-1 NPC cell line. At the concentration of 1 μM, 2ME2 was found to induce a short-term reversible G2/M cell-cycle arres... Full description

Journal Title: Cancer letters 2008, Vol.268 (2), p.295-307
Main Author: Lee, Yee-Man
Other Authors: Ting, Choi-Man , Cheng, Yuen-Kit , Fan, Tai-Ping , Wong, Ricky Ngok-Shun , Lung, Maria Li , Mak, Nai-Ki
Format: Electronic Article Electronic Article
Language: English
Subjects:
Quelle: Alma/SFX Local Collection
Publisher: Ireland: Elsevier Ireland Ltd
ID: ISSN: 0304-3835
Link: https://www.ncbi.nlm.nih.gov/pubmed/18492602
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title: Mechanisms of 2-methoxyestradiol-induced apoptosis and G2/M cell-cycle arrest of nasopharyngeal carcinoma cells
format: Article
creator:
  • Lee, Yee-Man
  • Ting, Choi-Man
  • Cheng, Yuen-Kit
  • Fan, Tai-Ping
  • Wong, Ricky Ngok-Shun
  • Lung, Maria Li
  • Mak, Nai-Ki
subjects:
  • 2-Methoxyestradiol
  • Antineoplastic Agents - pharmacology
  • Apoptosis
  • Apoptosis - drug effects
  • Cancer
  • Carcinoma
  • Cell cycle
  • Cell Division - drug effects
  • Cell Line, Tumor
  • Cell Proliferation - drug effects
  • Cell-cycle arrest
  • Cytoplasm
  • Estradiol - analogs & derivatives
  • Estradiol - pharmacology
  • Flow Cytometry
  • G2 Phase - drug effects
  • Hematology, Oncology and Palliative Medicine
  • Humans
  • JNK Mitogen-Activated Protein Kinases - metabolism
  • Kinases
  • MAP Kinase Signaling System - drug effects
  • Metastasis
  • Nasopharyngeal carcinoma
  • Nasopharyngeal Neoplasms - drug therapy
  • Nasopharyngeal Neoplasms - pathology
  • Oxidative Stress
  • Phosphorylation
  • Physiology
  • Proteins
  • Studies
  • Superoxide Dismutase - physiology
  • Tumors
ispartof: Cancer letters, 2008, Vol.268 (2), p.295-307
description: Abstract 2-Methoxyestradiol (2ME2) is an endogenous metabolite of 17β-estradiol (E2 ). This study aims to examine the anti-tumour activities of 2ME2 on the poorly differentiated HONE-1 NPC cell line. At the concentration of 1 μM, 2ME2 was found to induce a short-term reversible G2/M cell-cycle arrest. Further 10-fold increase to 10 μM, 2ME2 induced both irreversible G2/M phase cell-cycle arrest and apoptosis. Induction of apoptosis and G2/M cell-cycle arrest was due to oxidative stress as both apoptosis and the proportion of cells arresting at G2/M phase could be reduced by the superoxide dismutase (SOD) mimetic, TEMPO. Induction of apoptosis was accompanied with proteolytic cleavage of caspase-9 and -3, but not caspase-8. Kinetics studies revealed that 2ME2 induced a time-dependent inhibition of extracellular signal-regulated protein kinase (ERK) and an activation of c-jun N-terminal kinases (JNKs). The chemical inhibitor of JNKs, SP600125, was found to reduce 2ME2-induced apoptosis of the HONE-1 cells. Confocal microscopy revealed that the induction of G2/M cell-cycle arrest was associated with the presence of immunoreactivity of p-cdc2 (Tyr15) in the nucleus. The G2/M cell-cycle arrest is also correlated with an increased level of inactive p-cdc25C (Ser216) in 2ME2-treated HONE-1 cells. Results from this study indicate that production of superoxide anions might be involved in 2ME2-induced apoptosis and G2/M cell-cycle arrest of the HONE-1 cells.
language: eng
source: Alma/SFX Local Collection
identifier: ISSN: 0304-3835
fulltext: fulltext
issn:
  • 0304-3835
  • 1872-7980
url: Link


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descriptionAbstract 2-Methoxyestradiol (2ME2) is an endogenous metabolite of 17β-estradiol (E2 ). This study aims to examine the anti-tumour activities of 2ME2 on the poorly differentiated HONE-1 NPC cell line. At the concentration of 1 μM, 2ME2 was found to induce a short-term reversible G2/M cell-cycle arrest. Further 10-fold increase to 10 μM, 2ME2 induced both irreversible G2/M phase cell-cycle arrest and apoptosis. Induction of apoptosis and G2/M cell-cycle arrest was due to oxidative stress as both apoptosis and the proportion of cells arresting at G2/M phase could be reduced by the superoxide dismutase (SOD) mimetic, TEMPO. Induction of apoptosis was accompanied with proteolytic cleavage of caspase-9 and -3, but not caspase-8. Kinetics studies revealed that 2ME2 induced a time-dependent inhibition of extracellular signal-regulated protein kinase (ERK) and an activation of c-jun N-terminal kinases (JNKs). The chemical inhibitor of JNKs, SP600125, was found to reduce 2ME2-induced apoptosis of the HONE-1 cells. Confocal microscopy revealed that the induction of G2/M cell-cycle arrest was associated with the presence of immunoreactivity of p-cdc2 (Tyr15) in the nucleus. The G2/M cell-cycle arrest is also correlated with an increased level of inactive p-cdc25C (Ser216) in 2ME2-treated HONE-1 cells. Results from this study indicate that production of superoxide anions might be involved in 2ME2-induced apoptosis and G2/M cell-cycle arrest of the HONE-1 cells.
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subject2-Methoxyestradiol ; Antineoplastic Agents - pharmacology ; Apoptosis ; Apoptosis - drug effects ; Cancer ; Carcinoma ; Cell cycle ; Cell Division - drug effects ; Cell Line, Tumor ; Cell Proliferation - drug effects ; Cell-cycle arrest ; Cytoplasm ; Estradiol - analogs & derivatives ; Estradiol - pharmacology ; Flow Cytometry ; G2 Phase - drug effects ; Hematology, Oncology and Palliative Medicine ; Humans ; JNK Mitogen-Activated Protein Kinases - metabolism ; Kinases ; MAP Kinase Signaling System - drug effects ; Metastasis ; Nasopharyngeal carcinoma ; Nasopharyngeal Neoplasms - drug therapy ; Nasopharyngeal Neoplasms - pathology ; Oxidative Stress ; Phosphorylation ; Physiology ; Proteins ; Studies ; Superoxide Dismutase - physiology ; Tumors
ispartofCancer letters, 2008, Vol.268 (2), p.295-307
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descriptionAbstract 2-Methoxyestradiol (2ME2) is an endogenous metabolite of 17β-estradiol (E2 ). This study aims to examine the anti-tumour activities of 2ME2 on the poorly differentiated HONE-1 NPC cell line. At the concentration of 1 μM, 2ME2 was found to induce a short-term reversible G2/M cell-cycle arrest. Further 10-fold increase to 10 μM, 2ME2 induced both irreversible G2/M phase cell-cycle arrest and apoptosis. Induction of apoptosis and G2/M cell-cycle arrest was due to oxidative stress as both apoptosis and the proportion of cells arresting at G2/M phase could be reduced by the superoxide dismutase (SOD) mimetic, TEMPO. Induction of apoptosis was accompanied with proteolytic cleavage of caspase-9 and -3, but not caspase-8. Kinetics studies revealed that 2ME2 induced a time-dependent inhibition of extracellular signal-regulated protein kinase (ERK) and an activation of c-jun N-terminal kinases (JNKs). The chemical inhibitor of JNKs, SP600125, was found to reduce 2ME2-induced apoptosis of the HONE-1 cells. Confocal microscopy revealed that the induction of G2/M cell-cycle arrest was associated with the presence of immunoreactivity of p-cdc2 (Tyr15) in the nucleus. The G2/M cell-cycle arrest is also correlated with an increased level of inactive p-cdc25C (Ser216) in 2ME2-treated HONE-1 cells. Results from this study indicate that production of superoxide anions might be involved in 2ME2-induced apoptosis and G2/M cell-cycle arrest of the HONE-1 cells.
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25Oxidative Stress
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abstractAbstract 2-Methoxyestradiol (2ME2) is an endogenous metabolite of 17β-estradiol (E2 ). This study aims to examine the anti-tumour activities of 2ME2 on the poorly differentiated HONE-1 NPC cell line. At the concentration of 1 μM, 2ME2 was found to induce a short-term reversible G2/M cell-cycle arrest. Further 10-fold increase to 10 μM, 2ME2 induced both irreversible G2/M phase cell-cycle arrest and apoptosis. Induction of apoptosis and G2/M cell-cycle arrest was due to oxidative stress as both apoptosis and the proportion of cells arresting at G2/M phase could be reduced by the superoxide dismutase (SOD) mimetic, TEMPO. Induction of apoptosis was accompanied with proteolytic cleavage of caspase-9 and -3, but not caspase-8. Kinetics studies revealed that 2ME2 induced a time-dependent inhibition of extracellular signal-regulated protein kinase (ERK) and an activation of c-jun N-terminal kinases (JNKs). The chemical inhibitor of JNKs, SP600125, was found to reduce 2ME2-induced apoptosis of the HONE-1 cells. Confocal microscopy revealed that the induction of G2/M cell-cycle arrest was associated with the presence of immunoreactivity of p-cdc2 (Tyr15) in the nucleus. The G2/M cell-cycle arrest is also correlated with an increased level of inactive p-cdc25C (Ser216) in 2ME2-treated HONE-1 cells. Results from this study indicate that production of superoxide anions might be involved in 2ME2-induced apoptosis and G2/M cell-cycle arrest of the HONE-1 cells.
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