Dihydromyricetin induces apoptosis in a human choriocarcinoma cell line
Choriocarcinoma is a malignant trophoblastic tumor. The development of novel drugs is required to reduce the toxicity of current multi-agent chemotherapy and to successfully treat chemoresistant cases of the disease. The purpose of the present study was to investigate the effect of dihydromyricetin...
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Veröffentlicht in: | Oncology letters 2018-10, Vol.16 (4), p.4229-4234 |
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description | Choriocarcinoma is a malignant trophoblastic tumor. The development of novel drugs is required to reduce the toxicity of current multi-agent chemotherapy and to successfully treat chemoresistant cases of the disease. The purpose of the present study was to investigate the effect of dihydromyricetin (DMY) on the human choriocarcinoma cell line, JAr, to identify a novel drug for the treatment of choriocarcinoma. An MTT assay was performed to determine the effects of DMY at different concentrations and for different exposure durations. Flow cytometry and TUNEL assays were performed to detect apoptosis, and western blotting was utilized to investigate the underlying mechanism. The results revealed that DMY significantly inhibited JAr cell viability in a time- and dose-dependent manner. The flow cytometry and TUNEL assays demonstrated that DMY inhibited proliferation by inducing apoptosis. Further analysis by western blotting indicated that the protein expression level of BCL-2 associated X, associated protein increased, while the protein expression levels of BCL-2 and pro-caspase-3 decreased. These findings suggest that DMY induced apoptosis in human choriocarcinoma JAr cells, through a mitochondrially mediated apoptotic pathway. |
doi_str_mv | 10.3892/ol.2018.9220 |
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The development of novel drugs is required to reduce the toxicity of current multi-agent chemotherapy and to successfully treat chemoresistant cases of the disease. The purpose of the present study was to investigate the effect of dihydromyricetin (DMY) on the human choriocarcinoma cell line, JAr, to identify a novel drug for the treatment of choriocarcinoma. An MTT assay was performed to determine the effects of DMY at different concentrations and for different exposure durations. Flow cytometry and TUNEL assays were performed to detect apoptosis, and western blotting was utilized to investigate the underlying mechanism. The results revealed that DMY significantly inhibited JAr cell viability in a time- and dose-dependent manner. The flow cytometry and TUNEL assays demonstrated that DMY inhibited proliferation by inducing apoptosis. Further analysis by western blotting indicated that the protein expression level of BCL-2 associated X, associated protein increased, while the protein expression levels of BCL-2 and pro-caspase-3 decreased. These findings suggest that DMY induced apoptosis in human choriocarcinoma JAr cells, through a mitochondrially mediated apoptotic pathway.</description><identifier>ISSN: 1792-1074</identifier><identifier>EISSN: 1792-1082</identifier><identifier>DOI: 10.3892/ol.2018.9220</identifier><identifier>PMID: 30214558</identifier><language>eng</language><publisher>Greece: Spandidos Publications</publisher><subject>Apoptosis ; Cancer therapies ; Care and treatment ; Chemotherapy ; Choriocarcinoma ; Development and progression ; Drug dosages ; Flavonoids ; Flow cytometry ; Health aspects ; Lung cancer ; Morphology ; Oncology ; Protein expression ; Proteins</subject><ispartof>Oncology letters, 2018-10, Vol.16 (4), p.4229-4234</ispartof><rights>COPYRIGHT 2018 Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2018</rights><rights>Copyright: © Zuo et al. 2018</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c510t-8ff973ea9913000fd42ac99b591f9850edb0c244bf1bf503e1df8613aaa95cae3</citedby><cites>FETCH-LOGICAL-c510t-8ff973ea9913000fd42ac99b591f9850edb0c244bf1bf503e1df8613aaa95cae3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6126223/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6126223/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30214558$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zuo, Yanzhen</creatorcontrib><creatorcontrib>Xu, Qian</creatorcontrib><creatorcontrib>Lu, Yanjie</creatorcontrib><creatorcontrib>Sun, Dayong</creatorcontrib><creatorcontrib>Wang, Kang</creatorcontrib><creatorcontrib>Lei, Yuntao</creatorcontrib><creatorcontrib>Liang, Xiujun</creatorcontrib><creatorcontrib>Li, Yuhong</creatorcontrib><title>Dihydromyricetin induces apoptosis in a human choriocarcinoma cell line</title><title>Oncology letters</title><addtitle>Oncol Lett</addtitle><description>Choriocarcinoma is a malignant trophoblastic tumor. The development of novel drugs is required to reduce the toxicity of current multi-agent chemotherapy and to successfully treat chemoresistant cases of the disease. The purpose of the present study was to investigate the effect of dihydromyricetin (DMY) on the human choriocarcinoma cell line, JAr, to identify a novel drug for the treatment of choriocarcinoma. An MTT assay was performed to determine the effects of DMY at different concentrations and for different exposure durations. Flow cytometry and TUNEL assays were performed to detect apoptosis, and western blotting was utilized to investigate the underlying mechanism. The results revealed that DMY significantly inhibited JAr cell viability in a time- and dose-dependent manner. The flow cytometry and TUNEL assays demonstrated that DMY inhibited proliferation by inducing apoptosis. Further analysis by western blotting indicated that the protein expression level of BCL-2 associated X, associated protein increased, while the protein expression levels of BCL-2 and pro-caspase-3 decreased. These findings suggest that DMY induced apoptosis in human choriocarcinoma JAr cells, through a mitochondrially mediated apoptotic pathway.</description><subject>Apoptosis</subject><subject>Cancer therapies</subject><subject>Care and treatment</subject><subject>Chemotherapy</subject><subject>Choriocarcinoma</subject><subject>Development and progression</subject><subject>Drug dosages</subject><subject>Flavonoids</subject><subject>Flow cytometry</subject><subject>Health aspects</subject><subject>Lung cancer</subject><subject>Morphology</subject><subject>Oncology</subject><subject>Protein expression</subject><subject>Proteins</subject><issn>1792-1074</issn><issn>1792-1082</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>BENPR</sourceid><recordid>eNptkc9rFTEQx4MottTePMuC4Mn3zI_NbnIRStUqFLzoOcxmk25KNvNMdoX335tH67MPTA4ZZj7zZTJfQl4zuhVK8w8Yt5wytdWc02fknPWabxhV_Pkx7tszclnKPa1Hdkyp7iU5E5SzVkp1Tm4-hWk_Zpz3OVi3hNSENK7WlQZ2uFuwhFIzDTTTOkNq7IQ5oIVsQ8IZGutibGJI7hV54SEWd_n4XpCfXz7_uP66uf1-8-366nZjJaPLRnmve-FAaybqQH5sOVitB6mZ10pSNw7U8rYdPBu8pMKx0auOCQDQ0oITF-Tjg-5uHWY3WpeWDNHscpgh7w1CMKeVFCZzh79Nx3jHuagCbx8FMv5aXVnMPa451ZkNZ1TTnnLa_aPuIDoTkscqZudQrLmSslM91b2s1PY_VL2jm4PF5Hyo-ZOGd08aJgdxmQrGdQmYyin4_gG0GUvJzh9_yKg5OG8wmoPz5uB8xd883coR_uuz-APliKg3</recordid><startdate>20181001</startdate><enddate>20181001</enddate><creator>Zuo, Yanzhen</creator><creator>Xu, Qian</creator><creator>Lu, Yanjie</creator><creator>Sun, Dayong</creator><creator>Wang, Kang</creator><creator>Lei, Yuntao</creator><creator>Liang, Xiujun</creator><creator>Li, Yuhong</creator><general>Spandidos Publications</general><general>Spandidos Publications UK Ltd</general><general>D.A. 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The development of novel drugs is required to reduce the toxicity of current multi-agent chemotherapy and to successfully treat chemoresistant cases of the disease. The purpose of the present study was to investigate the effect of dihydromyricetin (DMY) on the human choriocarcinoma cell line, JAr, to identify a novel drug for the treatment of choriocarcinoma. An MTT assay was performed to determine the effects of DMY at different concentrations and for different exposure durations. Flow cytometry and TUNEL assays were performed to detect apoptosis, and western blotting was utilized to investigate the underlying mechanism. The results revealed that DMY significantly inhibited JAr cell viability in a time- and dose-dependent manner. The flow cytometry and TUNEL assays demonstrated that DMY inhibited proliferation by inducing apoptosis. Further analysis by western blotting indicated that the protein expression level of BCL-2 associated X, associated protein increased, while the protein expression levels of BCL-2 and pro-caspase-3 decreased. These findings suggest that DMY induced apoptosis in human choriocarcinoma JAr cells, through a mitochondrially mediated apoptotic pathway.</abstract><cop>Greece</cop><pub>Spandidos Publications</pub><pmid>30214558</pmid><doi>10.3892/ol.2018.9220</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Apoptosis Cancer therapies Care and treatment Chemotherapy Choriocarcinoma Development and progression Drug dosages Flavonoids Flow cytometry Health aspects Lung cancer Morphology Oncology Protein expression Proteins |
title | Dihydromyricetin induces apoptosis in a human choriocarcinoma cell line |
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