ApoG2 induces cell cycle arrest of nasopharyngeal carcinoma cells by suppressing the c-Myc signaling pathway

<p>Abstract</p> <p>Background</p> <p>apogossypolone (ApoG2) is a novel derivate of gossypol. We previously have reported that ApoG2 is a promising compound that kills nasopharyngeal carcinoma (NPC) cells by inhibiting the antiapoptotic function of Bcl-2 proteins. Howeve...

Full description

Bibliographic Details
Main Authors: Yang Dajun, Zhu Xiao-Feng, Sun Jian, Hu Zhe-Yu, Zeng Yi-Xin
Format: Article
Language:English
Published: BMC 2009-08-01
Series:Journal of Translational Medicine
Online Access:http://www.translational-medicine.com/content/7/1/74
_version_ 1811267008465993728
author Yang Dajun
Zhu Xiao-Feng
Sun Jian
Hu Zhe-Yu
Zeng Yi-Xin
author_facet Yang Dajun
Zhu Xiao-Feng
Sun Jian
Hu Zhe-Yu
Zeng Yi-Xin
author_sort Yang Dajun
collection DOAJ
description <p>Abstract</p> <p>Background</p> <p>apogossypolone (ApoG2) is a novel derivate of gossypol. We previously have reported that ApoG2 is a promising compound that kills nasopharyngeal carcinoma (NPC) cells by inhibiting the antiapoptotic function of Bcl-2 proteins. However, some researchers demonstrate that the antiproliferative effect of gossypol on breast cancer cells is mediated by induction of cell cycle arrest. So this study was aimed to investigate the effect of ApoG2 on cell cycle proliferation in NPC cells.</p> <p>Results</p> <p>We found that ApoG2 significantly suppressed the expression of c-Myc in NPC cells and induced arrest at the DNA synthesis (S) phase in a large percentage of NPC cells. Immunoblot analysis showed that expression of c-Myc protein was significantly downregulated by ApoG2 and that the expression of c-Myc's downstream molecules cyclin D1 and cyclin E were inhibited whereas p21 was induced. To further identify the cause-effect relationship between the suppression of c-Myc signaling pathway and induction of cell cycle arrest, the expression of c-Myc was interfered by siRNA. The results of cell cycle analysis showed that the downregulation of c-Myc signaling pathway by siRNA interference could cause a significant arrest of NPC cell at S phase of the cell cycle. In CNE-2 xenografts, ApoG2 significantly downregulated the expression of c-Myc and suppressed tumor growth <it>in vivo</it>.</p> <p>Conclusion</p> <p>Our findings indicated that ApoG2 could potently disturb the proliferation of NPC cells by suppressing c-Myc signaling pathway. This data suggested that the inhibitory effect of ApoG2 on NPC cell cycle proliferation might contribute to its use in anticancer therapy.</p>
first_indexed 2024-04-12T20:54:45Z
format Article
id doaj.art-75514dd0c874419abf91cdc9b909045d
institution Directory Open Access Journal
issn 1479-5876
language English
last_indexed 2024-04-12T20:54:45Z
publishDate 2009-08-01
publisher BMC
record_format Article
series Journal of Translational Medicine
spelling doaj.art-75514dd0c874419abf91cdc9b909045d2022-12-22T03:17:02ZengBMCJournal of Translational Medicine1479-58762009-08-01717410.1186/1479-5876-7-74ApoG2 induces cell cycle arrest of nasopharyngeal carcinoma cells by suppressing the c-Myc signaling pathwayYang DajunZhu Xiao-FengSun JianHu Zhe-YuZeng Yi-Xin<p>Abstract</p> <p>Background</p> <p>apogossypolone (ApoG2) is a novel derivate of gossypol. We previously have reported that ApoG2 is a promising compound that kills nasopharyngeal carcinoma (NPC) cells by inhibiting the antiapoptotic function of Bcl-2 proteins. However, some researchers demonstrate that the antiproliferative effect of gossypol on breast cancer cells is mediated by induction of cell cycle arrest. So this study was aimed to investigate the effect of ApoG2 on cell cycle proliferation in NPC cells.</p> <p>Results</p> <p>We found that ApoG2 significantly suppressed the expression of c-Myc in NPC cells and induced arrest at the DNA synthesis (S) phase in a large percentage of NPC cells. Immunoblot analysis showed that expression of c-Myc protein was significantly downregulated by ApoG2 and that the expression of c-Myc's downstream molecules cyclin D1 and cyclin E were inhibited whereas p21 was induced. To further identify the cause-effect relationship between the suppression of c-Myc signaling pathway and induction of cell cycle arrest, the expression of c-Myc was interfered by siRNA. The results of cell cycle analysis showed that the downregulation of c-Myc signaling pathway by siRNA interference could cause a significant arrest of NPC cell at S phase of the cell cycle. In CNE-2 xenografts, ApoG2 significantly downregulated the expression of c-Myc and suppressed tumor growth <it>in vivo</it>.</p> <p>Conclusion</p> <p>Our findings indicated that ApoG2 could potently disturb the proliferation of NPC cells by suppressing c-Myc signaling pathway. This data suggested that the inhibitory effect of ApoG2 on NPC cell cycle proliferation might contribute to its use in anticancer therapy.</p>http://www.translational-medicine.com/content/7/1/74
spellingShingle Yang Dajun
Zhu Xiao-Feng
Sun Jian
Hu Zhe-Yu
Zeng Yi-Xin
ApoG2 induces cell cycle arrest of nasopharyngeal carcinoma cells by suppressing the c-Myc signaling pathway
Journal of Translational Medicine
title ApoG2 induces cell cycle arrest of nasopharyngeal carcinoma cells by suppressing the c-Myc signaling pathway
title_full ApoG2 induces cell cycle arrest of nasopharyngeal carcinoma cells by suppressing the c-Myc signaling pathway
title_fullStr ApoG2 induces cell cycle arrest of nasopharyngeal carcinoma cells by suppressing the c-Myc signaling pathway
title_full_unstemmed ApoG2 induces cell cycle arrest of nasopharyngeal carcinoma cells by suppressing the c-Myc signaling pathway
title_short ApoG2 induces cell cycle arrest of nasopharyngeal carcinoma cells by suppressing the c-Myc signaling pathway
title_sort apog2 induces cell cycle arrest of nasopharyngeal carcinoma cells by suppressing the c myc signaling pathway
url http://www.translational-medicine.com/content/7/1/74
work_keys_str_mv AT yangdajun apog2inducescellcyclearrestofnasopharyngealcarcinomacellsbysuppressingthecmycsignalingpathway
AT zhuxiaofeng apog2inducescellcyclearrestofnasopharyngealcarcinomacellsbysuppressingthecmycsignalingpathway
AT sunjian apog2inducescellcyclearrestofnasopharyngealcarcinomacellsbysuppressingthecmycsignalingpathway
AT huzheyu apog2inducescellcyclearrestofnasopharyngealcarcinomacellsbysuppressingthecmycsignalingpathway
AT zengyixin apog2inducescellcyclearrestofnasopharyngealcarcinomacellsbysuppressingthecmycsignalingpathway