Journal Mobile Options
Table of Contents
Vol. 25, No. 2-3, 2010
Issue release date: 2010
Cell Physiol Biochem 2010;25:263–270
(DOI:10.1159/000276560)

External Qi of Yan Xin Qigong Induces Apoptosis and Inhibits Migration and Invasion of Estrogen-Independent Breast Cancer Cells Through Suppression of Akt/NF-ĸB Signaling

Yan X.1,2 · Shen H.2 · Jiang H.3 · Hu D.4 · Zhang C.5 · Wang J.2 · Wu X.3,4
1Chongqing Institute of Traditional Chinese Medicine, Chongqing,2New Medical Science Research Institute, New York,3Brigham and Women’s Hospital and Harvard Medical School, Boston,4Dana-Farber Cancer Institute and Harvard Medical School, Boston,5McMaster University, Hamilton
email Corresponding Author

Abstract

The antitumor effects of external Qi of Yan Xin Qigong (YXQ-EQ) have been widely described over the past three decades. To gain a better understanding of the mechanisms underlying YXQ-EQ’s antitumor effects, in the present study we investigated its effects on growth, migration, invasion and apoptosis of breast cancer cells and the underlying molecular mechanisms. We show that YXQ-EQ treatment caused a time-dependent reduction in viability, blocked clonogenic growth and induced apoptosis in estrogen-independent breast cancer MDA-MB-231 cells. Furthermore, YXQ-EQ treatment blocked migration and invasion of MDA-MB-231 cells. Biochemically, YXQ-EQ treatment markedly inhibited constitutive and EGF-induced Akt phosphorylation. YXQ-EQ also substantially repressed NF-ĸB activity, resulting in decreased expression of anti-apoptotic Bcl-2, Bcl-XL, XIAP and survivin proteins. These findings suggest that YXQ-EQ may induce apoptosis and inhibition of migration and invasion of MDA-MB-231 cells through the repression of Akt/NF-ĸB signaling.


 Outline


 goto top of outline Key Words

  • Breast cancer
  • Akt
  • NF-ĸB
  • External Qi of Yan Xin Qigong
  • Apoptosis
  • Metastasis

 goto top of outline Abstract

The antitumor effects of external Qi of Yan Xin Qigong (YXQ-EQ) have been widely described over the past three decades. To gain a better understanding of the mechanisms underlying YXQ-EQ’s antitumor effects, in the present study we investigated its effects on growth, migration, invasion and apoptosis of breast cancer cells and the underlying molecular mechanisms. We show that YXQ-EQ treatment caused a time-dependent reduction in viability, blocked clonogenic growth and induced apoptosis in estrogen-independent breast cancer MDA-MB-231 cells. Furthermore, YXQ-EQ treatment blocked migration and invasion of MDA-MB-231 cells. Biochemically, YXQ-EQ treatment markedly inhibited constitutive and EGF-induced Akt phosphorylation. YXQ-EQ also substantially repressed NF-ĸB activity, resulting in decreased expression of anti-apoptotic Bcl-2, Bcl-XL, XIAP and survivin proteins. These findings suggest that YXQ-EQ may induce apoptosis and inhibition of migration and invasion of MDA-MB-231 cells through the repression of Akt/NF-ĸB signaling.

Copyright © 2010 S. Karger AG, Basel


 goto top of outline Author Contacts

Xinqi Wu
Dana-Farber Cancer Institute and Harvard Medical School
44 Binney Street, Boston, MA 02115 (USA)
Tel. +1 617 582 8303, Fax: +1 617 582 7992
E-Mail xwu1@partners.org


 goto top of outline Article Information

Accepted: October 13, 2009
Published online: January 12, 2010
Number of Print Pages : 8


 goto top of outline Publication Details

Cellular Physiology and Biochemistry (International Journal of Experimental Cellular Physiology, Biochemistry and Pharmacology)

Vol. 25, No. 2-3, Year 2010 (Cover Date: 2010)

Journal Editor: F. Lang, Tübingen
ISSN: 1015–8987 (Print), eISSN: 1421–9778 (Online)

For additional information: http://www.karger.com/journals/cpb


Copyright / Drug Dosage / Disclaimer

Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher or, in the case of photocopying, direct payment of a specified fee to the Copyright Clearance Center.
Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in goverment regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug.
Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

Abstract

The antitumor effects of external Qi of Yan Xin Qigong (YXQ-EQ) have been widely described over the past three decades. To gain a better understanding of the mechanisms underlying YXQ-EQ’s antitumor effects, in the present study we investigated its effects on growth, migration, invasion and apoptosis of breast cancer cells and the underlying molecular mechanisms. We show that YXQ-EQ treatment caused a time-dependent reduction in viability, blocked clonogenic growth and induced apoptosis in estrogen-independent breast cancer MDA-MB-231 cells. Furthermore, YXQ-EQ treatment blocked migration and invasion of MDA-MB-231 cells. Biochemically, YXQ-EQ treatment markedly inhibited constitutive and EGF-induced Akt phosphorylation. YXQ-EQ also substantially repressed NF-ĸB activity, resulting in decreased expression of anti-apoptotic Bcl-2, Bcl-XL, XIAP and survivin proteins. These findings suggest that YXQ-EQ may induce apoptosis and inhibition of migration and invasion of MDA-MB-231 cells through the repression of Akt/NF-ĸB signaling.



 goto top of outline Author Contacts

Xinqi Wu
Dana-Farber Cancer Institute and Harvard Medical School
44 Binney Street, Boston, MA 02115 (USA)
Tel. +1 617 582 8303, Fax: +1 617 582 7992
E-Mail xwu1@partners.org


 goto top of outline Article Information

Accepted: October 13, 2009
Published online: January 12, 2010
Number of Print Pages : 8


 goto top of outline Publication Details

Cellular Physiology and Biochemistry (International Journal of Experimental Cellular Physiology, Biochemistry and Pharmacology)

Vol. 25, No. 2-3, Year 2010 (Cover Date: 2010)

Journal Editor: F. Lang, Tübingen
ISSN: 1015–8987 (Print), eISSN: 1421–9778 (Online)

For additional information: http://www.karger.com/journals/cpb


Copyright / Drug Dosage

Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher or, in the case of photocopying, direct payment of a specified fee to the Copyright Clearance Center.
Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in goverment regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug.
Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.