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Physalin A induces G2/M phase cell cycle arrest in human non-small cell lung cancer cells: involvement of the p38 MAPK/ROS pathway

Physalin A (PA) is an active withanolide isolated from Physalis alkekengi var . franchetii , a traditional Chinese herbal medicine named Jindenglong, which has long been used for the treatment of sore throat, hepatitis, and tumors in China. In the present study, we firstly investigated the effects o... Full description

Journal Title: Molecular and Cellular Biochemistry 2016, Vol.415(1), pp.145-155
Main Author: Kang, Ning
Other Authors: Jian, Jun-feng , Cao, Shi-jie , Zhang, Qiang , Mao, Yi-wei , Huang, Yi-yuan , Peng, Yan-fei , Qiu, Feng , Gao, Xiu-mei
Format: Electronic Article Electronic Article
Language: English
Subjects:
p38
ID: ISSN: 0300-8177 ; E-ISSN: 1573-4919 ; DOI: 10.1007/s11010-016-2686-1
Link: http://dx.doi.org/10.1007/s11010-016-2686-1
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recordid: springer_jour10.1007/s11010-016-2686-1
title: Physalin A induces G2/M phase cell cycle arrest in human non-small cell lung cancer cells: involvement of the p38 MAPK/ROS pathway
format: Article
creator:
  • Kang, Ning
  • Jian, Jun-feng
  • Cao, Shi-jie
  • Zhang, Qiang
  • Mao, Yi-wei
  • Huang, Yi-yuan
  • Peng, Yan-fei
  • Qiu, Feng
  • Gao, Xiu-mei
subjects:
  • Physalin A
  • G2/M cell cycle arrest
  • p38
  • Reactive oxygen species (ROS)
  • Non-small cell lung cancer (NSCLC)
ispartof: Molecular and Cellular Biochemistry, 2016, Vol.415(1), pp.145-155
description: Physalin A (PA) is an active withanolide isolated from Physalis alkekengi var . franchetii , a traditional Chinese herbal medicine named Jindenglong, which has long been used for the treatment of sore throat, hepatitis, and tumors in China. In the present study, we firstly investigated the effects of PA on proliferation and cell cycle distribution of the human non-small cell lung cancer (NSCLC) A549 cell line, and the potential mechanisms involved. Here, PA inhibited cell growth in dose- and time-dependent manners. Treatment of A549 cells with 28.4 μM PA for 24 h resulted in approximately 50 % cell death. PA increased the amount of intracellular ROS and the proportion of cells in G2/M. G2/M arrest was attenuated by the addition of ROS scavenger NAC. ERK and P38 were triggered by PA through phosphorylation in a time-dependent manner. The phosphorylation of ERK and P38 were not attenuated by the addition of NAC, but the use of the p38 inhibitor could reduce, at least in part, PA-induced ROS and the proportion of cells in G2/M. PA induces G2/M cell cycle arrest in A549 cells involving in the p38 MAPK/ROS pathway. This study suggests that PA might be a promising therapeutic agent against NSCLC.
language: eng
source:
identifier: ISSN: 0300-8177 ; E-ISSN: 1573-4919 ; DOI: 10.1007/s11010-016-2686-1
fulltext: fulltext
issn:
  • 1573-4919
  • 15734919
  • 0300-8177
  • 03008177
url: Link


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titlePhysalin A induces G2/M phase cell cycle arrest in human non-small cell lung cancer cells: involvement of the p38 MAPK/ROS pathway
creatorKang, Ning ; Jian, Jun-feng ; Cao, Shi-jie ; Zhang, Qiang ; Mao, Yi-wei ; Huang, Yi-yuan ; Peng, Yan-fei ; Qiu, Feng ; Gao, Xiu-mei
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subjectPhysalin A ; G2/M cell cycle arrest ; p38 ; Reactive oxygen species (ROS) ; Non-small cell lung cancer (NSCLC)
descriptionPhysalin A (PA) is an active withanolide isolated from Physalis alkekengi var . franchetii , a traditional Chinese herbal medicine named Jindenglong, which has long been used for the treatment of sore throat, hepatitis, and tumors in China. In the present study, we firstly investigated the effects of PA on proliferation and cell cycle distribution of the human non-small cell lung cancer (NSCLC) A549 cell line, and the potential mechanisms involved. Here, PA inhibited cell growth in dose- and time-dependent manners. Treatment of A549 cells with 28.4 μM PA for 24 h resulted in approximately 50 % cell death. PA increased the amount of intracellular ROS and the proportion of cells in G2/M. G2/M arrest was attenuated by the addition of ROS scavenger NAC. ERK and P38 were triggered by PA through phosphorylation in a time-dependent manner. The phosphorylation of ERK and P38 were not attenuated by the addition of NAC, but the use of the p38 inhibitor could reduce, at least in part, PA-induced ROS and the proportion of cells in G2/M. PA induces G2/M cell cycle arrest in A549 cells involving in the p38 MAPK/ROS pathway. This study suggests that PA might be a promising therapeutic agent against NSCLC.
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titlePhysalin A induces G2/M phase cell cycle arrest in human non-small cell lung cancer cells: involvement of the p38 MAPK/ROS pathway
descriptionPhysalin A (PA) is an active withanolide isolated from Physalis alkekengi var . franchetii , a traditional Chinese herbal medicine named Jindenglong, which has long been used for the treatment of sore throat, hepatitis, and tumors in China. In the present study, we firstly investigated the effects of PA on proliferation and cell cycle distribution of the human non-small cell lung cancer (NSCLC) A549 cell line, and the potential mechanisms involved. Here, PA inhibited cell growth in dose- and time-dependent manners. Treatment of A549 cells with 28.4 μM PA for 24 h resulted in approximately 50 % cell death. PA increased the amount of intracellular ROS and the proportion of cells in G2/M. G2/M arrest was attenuated by the addition of ROS scavenger NAC. ERK and P38 were triggered by PA through phosphorylation in a time-dependent manner. The phosphorylation of ERK and P38 were not attenuated by the addition of NAC, but the use of the p38 inhibitor could reduce, at least in part, PA-induced ROS and the proportion of cells in G2/M. PA induces G2/M cell cycle arrest in A549 cells involving in the p38 MAPK/ROS pathway. This study suggests that PA might be a promising therapeutic agent against NSCLC.
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abstractPhysalin A (PA) is an active withanolide isolated from Physalis alkekengi var . franchetii , a traditional Chinese herbal medicine named Jindenglong, which has long been used for the treatment of sore throat, hepatitis, and tumors in China. In the present study, we firstly investigated the effects of PA on proliferation and cell cycle distribution of the human non-small cell lung cancer (NSCLC) A549 cell line, and the potential mechanisms involved. Here, PA inhibited cell growth in dose- and time-dependent manners. Treatment of A549 cells with 28.4 μM PA for 24 h resulted in approximately 50 % cell death. PA increased the amount of intracellular ROS and the proportion of cells in G2/M. G2/M arrest was attenuated by the addition of ROS scavenger NAC. ERK and P38 were triggered by PA through phosphorylation in a time-dependent manner. The phosphorylation of ERK and P38 were not attenuated by the addition of NAC, but the use of the p38 inhibitor could reduce, at least in part, PA-induced ROS and the proportion of cells in G2/M. PA induces G2/M cell cycle arrest in A549 cells involving in the p38 MAPK/ROS pathway. This study suggests that PA might be a promising therapeutic agent against NSCLC.
copNew York
pubSpringer US
doi10.1007/s11010-016-2686-1
pages145-155
date2016-04