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...
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Format: | Article |
Language: | English |
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BMC
2009-08-01
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Series: | Journal of Translational Medicine |
Online Access: | http://www.translational-medicine.com/content/7/1/74 |
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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> |
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issn | 1479-5876 |
language | English |
last_indexed | 2024-04-12T20:54:45Z |
publishDate | 2009-08-01 |
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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 |
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