Correction of malignant behavior of tumor cells by traditional Chinese herb medicine through a restoration of p53
We have previously demonstrated that a UVC-induced tumorigenic HeLa x skin fibroblast cell line could be induced to form a more normal phenotypic state (‘reversion’), including loss of IAP expression. We have now used the loss of IAP expression to monitor the enhancement of this reversion in the cer...
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| Veröffentlicht in: | Cancer letters 2006-02, Vol.233 (2), p.315-327 |
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| creator | Deng, Win-Ping Chao, Ming-Wei Lai, Wen-Fu Sun, Chi Chung, Chen-Yen Wu, Cheng-Chia Lin, I-Hsin Hwang, Jeng-Jong Wu, Chiu-Hsiung Chiu, Wen-Ta Chen, Chia-Yu Redpath, John-Leslie |
| description | We have previously demonstrated that a UVC-induced tumorigenic HeLa x skin fibroblast cell line could be induced to form a more normal phenotypic state (‘reversion’), including loss of IAP expression. We have now used the loss of IAP expression to monitor the enhancement of this reversion in the cervical cancer cell line, HeLa, by a traditional Chinese herb medicine (TCM), Yigan Kang (YGK). IAP level decreased, and the reversion frequency increased, in a dose-dependent manner at concentrations of YGK of more than 10
mg. YGK significantly repressed E6/E7 oncogenes at the transcriptional level, with subsequent reactivation of p53 and p21 expression (
P |
| doi_str_mv | 10.1016/j.canlet.2005.03.031 |
| format | Article |
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mg. YGK significantly repressed E6/E7 oncogenes at the transcriptional level, with subsequent reactivation of p53 and p21 expression (
P<0.01). YGK had little effect on the cell cycle of HeLa cells and slightly increased the apoptotic cell death between 20 and 40
mg. In vivo, tumorigenicity studies were performed using six different animal experimental protocols, which demonstrated that YGK was effective at inducing reversion of the tumorigenic phenotype, with YGK-treated HeLa cells showing much less aggressive tumor growth than untreated cells. YGK may raise the possibility of the continuing management of some cancers as a chronic condition in which the malignant behavior of the tumor cells is constrained.</description><identifier>ISSN: 0304-3835</identifier><identifier>EISSN: 1872-7980</identifier><identifier>DOI: 10.1016/j.canlet.2005.03.031</identifier><identifier>PMID: 15882924</identifier><language>eng</language><publisher>Ireland: Elsevier Ireland Ltd</publisher><subject>Alkaline Phosphatase - metabolism ; Animals ; Cancer reversion ; Cell Cycle - drug effects ; Cell Proliferation - drug effects ; Cell Survival - drug effects ; Cell Transformation, Neoplastic - drug effects ; Cell Transformation, Neoplastic - metabolism ; Cervical cancer ; Experiments ; Genotype & phenotype ; HeLa Cells - drug effects ; HeLa Cells - pathology ; Hepatitis ; HPV ; Human papillomavirus ; Humans ; IAP ; Intestines - enzymology ; Medicine, Chinese Traditional ; Mice ; Mice, Inbred NOD ; Mice, SCID ; p53 ; Studies ; TCM ; Tumor Suppressor Protein p53 - genetics ; Tumor Suppressor Protein p53 - metabolism ; Tumors ; Yigan Kang</subject><ispartof>Cancer letters, 2006-02, Vol.233 (2), p.315-327</ispartof><rights>2005 Elsevier Ireland Ltd</rights><rights>Copyright Elsevier Limited Feb 28, 2006</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c454t-628f2661fbdaee6eede804a06a2d3200c8d5bf8d0ab27798f09b89d9b0257dad3</citedby><cites>FETCH-LOGICAL-c454t-628f2661fbdaee6eede804a06a2d3200c8d5bf8d0ab27798f09b89d9b0257dad3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.canlet.2005.03.031$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15882924$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Deng, Win-Ping</creatorcontrib><creatorcontrib>Chao, Ming-Wei</creatorcontrib><creatorcontrib>Lai, Wen-Fu</creatorcontrib><creatorcontrib>Sun, Chi</creatorcontrib><creatorcontrib>Chung, Chen-Yen</creatorcontrib><creatorcontrib>Wu, Cheng-Chia</creatorcontrib><creatorcontrib>Lin, I-Hsin</creatorcontrib><creatorcontrib>Hwang, Jeng-Jong</creatorcontrib><creatorcontrib>Wu, Chiu-Hsiung</creatorcontrib><creatorcontrib>Chiu, Wen-Ta</creatorcontrib><creatorcontrib>Chen, Chia-Yu</creatorcontrib><creatorcontrib>Redpath, John-Leslie</creatorcontrib><title>Correction of malignant behavior of tumor cells by traditional Chinese herb medicine through a restoration of p53</title><title>Cancer letters</title><addtitle>Cancer Lett</addtitle><description>We have previously demonstrated that a UVC-induced tumorigenic HeLa x skin fibroblast cell line could be induced to form a more normal phenotypic state (‘reversion’), including loss of IAP expression. We have now used the loss of IAP expression to monitor the enhancement of this reversion in the cervical cancer cell line, HeLa, by a traditional Chinese herb medicine (TCM), Yigan Kang (YGK). IAP level decreased, and the reversion frequency increased, in a dose-dependent manner at concentrations of YGK of more than 10
mg. YGK significantly repressed E6/E7 oncogenes at the transcriptional level, with subsequent reactivation of p53 and p21 expression (
P<0.01). YGK had little effect on the cell cycle of HeLa cells and slightly increased the apoptotic cell death between 20 and 40
mg. In vivo, tumorigenicity studies were performed using six different animal experimental protocols, which demonstrated that YGK was effective at inducing reversion of the tumorigenic phenotype, with YGK-treated HeLa cells showing much less aggressive tumor growth than untreated cells. 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Chao, Ming-Wei ; Lai, Wen-Fu ; Sun, Chi ; Chung, Chen-Yen ; Wu, Cheng-Chia ; Lin, I-Hsin ; Hwang, Jeng-Jong ; Wu, Chiu-Hsiung ; Chiu, Wen-Ta ; Chen, Chia-Yu ; Redpath, John-Leslie</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c454t-628f2661fbdaee6eede804a06a2d3200c8d5bf8d0ab27798f09b89d9b0257dad3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Alkaline Phosphatase - metabolism</topic><topic>Animals</topic><topic>Cancer reversion</topic><topic>Cell Cycle - drug effects</topic><topic>Cell Proliferation - drug effects</topic><topic>Cell Survival - drug effects</topic><topic>Cell Transformation, Neoplastic - drug effects</topic><topic>Cell Transformation, Neoplastic - metabolism</topic><topic>Cervical cancer</topic><topic>Experiments</topic><topic>Genotype & phenotype</topic><topic>HeLa Cells - drug effects</topic><topic>HeLa Cells - pathology</topic><topic>Hepatitis</topic><topic>HPV</topic><topic>Human papillomavirus</topic><topic>Humans</topic><topic>IAP</topic><topic>Intestines - enzymology</topic><topic>Medicine, Chinese Traditional</topic><topic>Mice</topic><topic>Mice, Inbred NOD</topic><topic>Mice, SCID</topic><topic>p53</topic><topic>Studies</topic><topic>TCM</topic><topic>Tumor Suppressor Protein p53 - genetics</topic><topic>Tumor Suppressor Protein p53 - metabolism</topic><topic>Tumors</topic><topic>Yigan Kang</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Deng, Win-Ping</creatorcontrib><creatorcontrib>Chao, Ming-Wei</creatorcontrib><creatorcontrib>Lai, Wen-Fu</creatorcontrib><creatorcontrib>Sun, Chi</creatorcontrib><creatorcontrib>Chung, Chen-Yen</creatorcontrib><creatorcontrib>Wu, Cheng-Chia</creatorcontrib><creatorcontrib>Lin, I-Hsin</creatorcontrib><creatorcontrib>Hwang, Jeng-Jong</creatorcontrib><creatorcontrib>Wu, Chiu-Hsiung</creatorcontrib><creatorcontrib>Chiu, Wen-Ta</creatorcontrib><creatorcontrib>Chen, Chia-Yu</creatorcontrib><creatorcontrib>Redpath, John-Leslie</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><collection>MEDLINE - Academic</collection><jtitle>Cancer letters</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Deng, Win-Ping</au><au>Chao, Ming-Wei</au><au>Lai, Wen-Fu</au><au>Sun, Chi</au><au>Chung, Chen-Yen</au><au>Wu, Cheng-Chia</au><au>Lin, I-Hsin</au><au>Hwang, Jeng-Jong</au><au>Wu, Chiu-Hsiung</au><au>Chiu, Wen-Ta</au><au>Chen, Chia-Yu</au><au>Redpath, John-Leslie</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Correction of malignant behavior of tumor cells by traditional Chinese herb medicine through a restoration of p53</atitle><jtitle>Cancer letters</jtitle><addtitle>Cancer Lett</addtitle><date>2006-02-28</date><risdate>2006</risdate><volume>233</volume><issue>2</issue><spage>315</spage><epage>327</epage><pages>315-327</pages><issn>0304-3835</issn><eissn>1872-7980</eissn><abstract>We have previously demonstrated that a UVC-induced tumorigenic HeLa x skin fibroblast cell line could be induced to form a more normal phenotypic state (‘reversion’), including loss of IAP expression. 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mg. YGK significantly repressed E6/E7 oncogenes at the transcriptional level, with subsequent reactivation of p53 and p21 expression (
P<0.01). YGK had little effect on the cell cycle of HeLa cells and slightly increased the apoptotic cell death between 20 and 40
mg. In vivo, tumorigenicity studies were performed using six different animal experimental protocols, which demonstrated that YGK was effective at inducing reversion of the tumorigenic phenotype, with YGK-treated HeLa cells showing much less aggressive tumor growth than untreated cells. YGK may raise the possibility of the continuing management of some cancers as a chronic condition in which the malignant behavior of the tumor cells is constrained.</abstract><cop>Ireland</cop><pub>Elsevier Ireland Ltd</pub><pmid>15882924</pmid><doi>10.1016/j.canlet.2005.03.031</doi><tpages>13</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0304-3835 |
| ispartof | Cancer letters, 2006-02, Vol.233 (2), p.315-327 |
| issn | 0304-3835 1872-7980 |
| language | eng |
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| source | MEDLINE; ScienceDirect Journals (5 years ago - present) |
| subjects | Alkaline Phosphatase - metabolism Animals Cancer reversion Cell Cycle - drug effects Cell Proliferation - drug effects Cell Survival - drug effects Cell Transformation, Neoplastic - drug effects Cell Transformation, Neoplastic - metabolism Cervical cancer Experiments Genotype & phenotype HeLa Cells - drug effects HeLa Cells - pathology Hepatitis HPV Human papillomavirus Humans IAP Intestines - enzymology Medicine, Chinese Traditional Mice Mice, Inbred NOD Mice, SCID p53 Studies TCM Tumor Suppressor Protein p53 - genetics Tumor Suppressor Protein p53 - metabolism Tumors Yigan Kang |
| title | Correction of malignant behavior of tumor cells by traditional Chinese herb medicine through a restoration of p53 |
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