Effects of ginsenoside Rg3 on epigenetic modification in ovarian cancer cells
Epigenetic modifications are closely related to oncogene activation and tumor suppressor gene inactivation. The aim of this study was to determine the effects of ginsenoside Rg3 on epigenetic modification in ovarian cancer cells. Cell proliferation, metastasis, invasion and apoptosis were respective...
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| Veröffentlicht in: | Oncology reports 2019-06, Vol.41 (6), p.3209-3218 |
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| creator | Zhao, Lingqin Shou, Huafeng Chen, Lu Gao, Wen Fang, Chenyan Zhang, Ping |
| description | Epigenetic modifications are closely related to oncogene activation and tumor suppressor gene inactivation. The aim of this study was to determine the effects of ginsenoside Rg3 on epigenetic modification in ovarian cancer cells. Cell proliferation, metastasis, invasion and apoptosis were respectively determined using Cell Counting Kit‑8 (CCK‑8), wound healing, Transwell and flow cytometric assays. Methylation levels were determined using methylation specific PCR (MSP). Related‑factor expression was detected by conducting real‑time‑qPCR (RT‑qPCR) and western blotting. The results revealed that cell proliferation was inhibited by ginsenoside Rg3 (0, 25, 50, 100 and 200 µg/ml) in a time‑dependent manner (12, 24 and 48 h). Ginsenoside Rg3 (50, 100 and 200 µg/ml) was selected to treat cells in various experiments. When ovarian cells were treated with ginsenoside Rg3, cell apoptosis was observed to be promoted, while cell metastasis and invasion were inhibited at 48 h. The results of the present study revealed that in the promoter regions of p53, p16 and hMLH1, the methylation levels decreased, while the mRNA and protein levels significantly increased. The activities of DNMTs and mRNA as well as protein levels of DNMT1, DNMT3a and DNMT3b were decreased by Rg3. The data also demonstrated that the mRNA and protein levels of acetyl‑H3 K14/K9 and acetyl‑H4 K12/K5/K16 were increased by Rg3. Hence, ginsenoside Rg3 inhibited ovarian cancer cell viability, migration and invasion as well as promoted cell apoptosis. |
| doi_str_mv | 10.3892/or.2019.7115 |
| format | Article |
| fullrecord | <record><control><sourceid>gale_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_6489025</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A585353877</galeid><sourcerecordid>A585353877</sourcerecordid><originalsourceid>FETCH-LOGICAL-c510t-860f63c8e9a664bb7b9eab09c9ed7e29d033496813dde2419c39a7060cb3de4b3</originalsourceid><addsrcrecordid>eNptkd1LHDEUxUOpdO3qW59LoNAnZ83HfOWlIKJVUARR8C1kkpvZLDPJNpkV-t83y1p1QfKQy83vHm7OQegbJQveCnYa4oIRKhYNpdUndEgbQQtWcvo514TRgvPqaYa-prQihDWkFl_QjNNc84ofotsLa0FPCQeLe-cT-JCcAXzfcxw8hrXrwcPkNB6DcdZpNbncdx6HZxWd8lgrryFiDcOQjtCBVUOC45d7jh4vLx7Or4qbu9_X52c3ha4omYq2JrbmugWh6rrsuqYToDoitADTABOGcF6KuqXcGGAlFZoLlVcnuuMGyo7P0a-d7nrTjWA0-CmqQa6jG1X8K4Nycv_Fu6Xsw7Osy1YQVmWBHy8CMfzZQJrkKmyizztLxmhL66psxBvVqwGk8zZkMT26pOVZ1VbZwLZpMrX4gMrHwOh08GBd7u8N_Hw3sAQ1TMsUhs3W2bQPnuxAHUNKEezrDymR2_BliHIbvtyGn_Hv7115hf-nzf8BYZ6ozQ</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2218165479</pqid></control><display><type>article</type><title>Effects of ginsenoside Rg3 on epigenetic modification in ovarian cancer cells</title><source>MEDLINE</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>Alma/SFX Local Collection</source><creator>Zhao, Lingqin ; Shou, Huafeng ; Chen, Lu ; Gao, Wen ; Fang, Chenyan ; Zhang, Ping</creator><creatorcontrib>Zhao, Lingqin ; Shou, Huafeng ; Chen, Lu ; Gao, Wen ; Fang, Chenyan ; Zhang, Ping</creatorcontrib><description>Epigenetic modifications are closely related to oncogene activation and tumor suppressor gene inactivation. The aim of this study was to determine the effects of ginsenoside Rg3 on epigenetic modification in ovarian cancer cells. Cell proliferation, metastasis, invasion and apoptosis were respectively determined using Cell Counting Kit‑8 (CCK‑8), wound healing, Transwell and flow cytometric assays. Methylation levels were determined using methylation specific PCR (MSP). Related‑factor expression was detected by conducting real‑time‑qPCR (RT‑qPCR) and western blotting. The results revealed that cell proliferation was inhibited by ginsenoside Rg3 (0, 25, 50, 100 and 200 µg/ml) in a time‑dependent manner (12, 24 and 48 h). Ginsenoside Rg3 (50, 100 and 200 µg/ml) was selected to treat cells in various experiments. When ovarian cells were treated with ginsenoside Rg3, cell apoptosis was observed to be promoted, while cell metastasis and invasion were inhibited at 48 h. The results of the present study revealed that in the promoter regions of p53, p16 and hMLH1, the methylation levels decreased, while the mRNA and protein levels significantly increased. The activities of DNMTs and mRNA as well as protein levels of DNMT1, DNMT3a and DNMT3b were decreased by Rg3. The data also demonstrated that the mRNA and protein levels of acetyl‑H3 K14/K9 and acetyl‑H4 K12/K5/K16 were increased by Rg3. Hence, ginsenoside Rg3 inhibited ovarian cancer cell viability, migration and invasion as well as promoted cell apoptosis.</description><identifier>ISSN: 1021-335X</identifier><identifier>EISSN: 1791-2431</identifier><identifier>DOI: 10.3892/or.2019.7115</identifier><identifier>PMID: 31002353</identifier><language>eng</language><publisher>Greece: Spandidos Publications</publisher><subject>Apoptosis ; Apoptosis - drug effects ; Cancer cells ; Cancer metastasis ; Cancer therapies ; Care and treatment ; Cell cycle ; Cell growth ; Cell Line, Tumor ; Cell Proliferation - drug effects ; Cell Survival - drug effects ; Cyclin-Dependent Kinase Inhibitor p16 - genetics ; Deoxyribonucleic acid ; DNA ; DNA (Cytosine-5-)-Methyltransferase 1 - genetics ; DNA (Cytosine-5-)-Methyltransferases - genetics ; DNA methylation ; DNA Methylation - genetics ; DNA Methyltransferase 3A ; DNA Methyltransferase 3B ; Dosage and administration ; Epigenesis, Genetic ; Epigenetic inheritance ; Epigenetics ; Female ; Gene Expression Regulation, Neoplastic - drug effects ; Genes ; Genetic aspects ; Ginsenosides - pharmacology ; Health aspects ; Humans ; Medical prognosis ; Messenger RNA ; Metastasis ; Methylation ; Methyltransferases ; Mortality ; MutL Protein Homolog 1 - genetics ; Ovarian cancer ; Ovarian Neoplasms - drug therapy ; Ovarian Neoplasms - genetics ; Ovarian Neoplasms - pathology ; Physiological aspects ; Polymerase chain reaction ; Post-translational modifications ; RNA ; Saponins ; Signal Transduction - drug effects ; Tumor proteins ; Tumor suppressor genes ; Tumor Suppressor Protein p53 - genetics ; Tumors ; Wound care ; Wound healing</subject><ispartof>Oncology reports, 2019-06, Vol.41 (6), p.3209-3218</ispartof><rights>COPYRIGHT 2019 Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2019</rights><rights>Copyright: © Zhao et al. 2019</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c510t-860f63c8e9a664bb7b9eab09c9ed7e29d033496813dde2419c39a7060cb3de4b3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,776,780,881,27903,27904</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31002353$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhao, Lingqin</creatorcontrib><creatorcontrib>Shou, Huafeng</creatorcontrib><creatorcontrib>Chen, Lu</creatorcontrib><creatorcontrib>Gao, Wen</creatorcontrib><creatorcontrib>Fang, Chenyan</creatorcontrib><creatorcontrib>Zhang, Ping</creatorcontrib><title>Effects of ginsenoside Rg3 on epigenetic modification in ovarian cancer cells</title><title>Oncology reports</title><addtitle>Oncol Rep</addtitle><description>Epigenetic modifications are closely related to oncogene activation and tumor suppressor gene inactivation. The aim of this study was to determine the effects of ginsenoside Rg3 on epigenetic modification in ovarian cancer cells. Cell proliferation, metastasis, invasion and apoptosis were respectively determined using Cell Counting Kit‑8 (CCK‑8), wound healing, Transwell and flow cytometric assays. Methylation levels were determined using methylation specific PCR (MSP). Related‑factor expression was detected by conducting real‑time‑qPCR (RT‑qPCR) and western blotting. The results revealed that cell proliferation was inhibited by ginsenoside Rg3 (0, 25, 50, 100 and 200 µg/ml) in a time‑dependent manner (12, 24 and 48 h). Ginsenoside Rg3 (50, 100 and 200 µg/ml) was selected to treat cells in various experiments. When ovarian cells were treated with ginsenoside Rg3, cell apoptosis was observed to be promoted, while cell metastasis and invasion were inhibited at 48 h. The results of the present study revealed that in the promoter regions of p53, p16 and hMLH1, the methylation levels decreased, while the mRNA and protein levels significantly increased. The activities of DNMTs and mRNA as well as protein levels of DNMT1, DNMT3a and DNMT3b were decreased by Rg3. The data also demonstrated that the mRNA and protein levels of acetyl‑H3 K14/K9 and acetyl‑H4 K12/K5/K16 were increased by Rg3. Hence, ginsenoside Rg3 inhibited ovarian cancer cell viability, migration and invasion as well as promoted cell apoptosis.</description><subject>Apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>Cancer cells</subject><subject>Cancer metastasis</subject><subject>Cancer therapies</subject><subject>Care and treatment</subject><subject>Cell cycle</subject><subject>Cell growth</subject><subject>Cell Line, Tumor</subject><subject>Cell Proliferation - drug effects</subject><subject>Cell Survival - drug effects</subject><subject>Cyclin-Dependent Kinase Inhibitor p16 - genetics</subject><subject>Deoxyribonucleic acid</subject><subject>DNA</subject><subject>DNA (Cytosine-5-)-Methyltransferase 1 - genetics</subject><subject>DNA (Cytosine-5-)-Methyltransferases - genetics</subject><subject>DNA methylation</subject><subject>DNA Methylation - genetics</subject><subject>DNA Methyltransferase 3A</subject><subject>DNA Methyltransferase 3B</subject><subject>Dosage and administration</subject><subject>Epigenesis, Genetic</subject><subject>Epigenetic inheritance</subject><subject>Epigenetics</subject><subject>Female</subject><subject>Gene Expression Regulation, Neoplastic - drug effects</subject><subject>Genes</subject><subject>Genetic aspects</subject><subject>Ginsenosides - pharmacology</subject><subject>Health aspects</subject><subject>Humans</subject><subject>Medical prognosis</subject><subject>Messenger RNA</subject><subject>Metastasis</subject><subject>Methylation</subject><subject>Methyltransferases</subject><subject>Mortality</subject><subject>MutL Protein Homolog 1 - genetics</subject><subject>Ovarian cancer</subject><subject>Ovarian Neoplasms - drug therapy</subject><subject>Ovarian Neoplasms - genetics</subject><subject>Ovarian Neoplasms - pathology</subject><subject>Physiological aspects</subject><subject>Polymerase chain reaction</subject><subject>Post-translational modifications</subject><subject>RNA</subject><subject>Saponins</subject><subject>Signal Transduction - drug effects</subject><subject>Tumor proteins</subject><subject>Tumor suppressor genes</subject><subject>Tumor Suppressor Protein p53 - genetics</subject><subject>Tumors</subject><subject>Wound care</subject><subject>Wound healing</subject><issn>1021-335X</issn><issn>1791-2431</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNptkd1LHDEUxUOpdO3qW59LoNAnZ83HfOWlIKJVUARR8C1kkpvZLDPJNpkV-t83y1p1QfKQy83vHm7OQegbJQveCnYa4oIRKhYNpdUndEgbQQtWcvo514TRgvPqaYa-prQihDWkFl_QjNNc84ofotsLa0FPCQeLe-cT-JCcAXzfcxw8hrXrwcPkNB6DcdZpNbncdx6HZxWd8lgrryFiDcOQjtCBVUOC45d7jh4vLx7Or4qbu9_X52c3ha4omYq2JrbmugWh6rrsuqYToDoitADTABOGcF6KuqXcGGAlFZoLlVcnuuMGyo7P0a-d7nrTjWA0-CmqQa6jG1X8K4Nycv_Fu6Xsw7Osy1YQVmWBHy8CMfzZQJrkKmyizztLxmhL66psxBvVqwGk8zZkMT26pOVZ1VbZwLZpMrX4gMrHwOh08GBd7u8N_Hw3sAQ1TMsUhs3W2bQPnuxAHUNKEezrDymR2_BliHIbvtyGn_Hv7115hf-nzf8BYZ6ozQ</recordid><startdate>20190601</startdate><enddate>20190601</enddate><creator>Zhao, Lingqin</creator><creator>Shou, Huafeng</creator><creator>Chen, Lu</creator><creator>Gao, Wen</creator><creator>Fang, Chenyan</creator><creator>Zhang, Ping</creator><general>Spandidos Publications</general><general>Spandidos Publications UK Ltd</general><general>D.A. Spandidos</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AN0</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>5PM</scope></search><sort><creationdate>20190601</creationdate><title>Effects of ginsenoside Rg3 on epigenetic modification in ovarian cancer cells</title><author>Zhao, Lingqin ; Shou, Huafeng ; Chen, Lu ; Gao, Wen ; Fang, Chenyan ; Zhang, Ping</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c510t-860f63c8e9a664bb7b9eab09c9ed7e29d033496813dde2419c39a7060cb3de4b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Apoptosis</topic><topic>Apoptosis - drug effects</topic><topic>Cancer cells</topic><topic>Cancer metastasis</topic><topic>Cancer therapies</topic><topic>Care and treatment</topic><topic>Cell cycle</topic><topic>Cell growth</topic><topic>Cell Line, Tumor</topic><topic>Cell Proliferation - drug effects</topic><topic>Cell Survival - drug effects</topic><topic>Cyclin-Dependent Kinase Inhibitor p16 - genetics</topic><topic>Deoxyribonucleic acid</topic><topic>DNA</topic><topic>DNA (Cytosine-5-)-Methyltransferase 1 - genetics</topic><topic>DNA (Cytosine-5-)-Methyltransferases - genetics</topic><topic>DNA methylation</topic><topic>DNA Methylation - genetics</topic><topic>DNA Methyltransferase 3A</topic><topic>DNA Methyltransferase 3B</topic><topic>Dosage and administration</topic><topic>Epigenesis, Genetic</topic><topic>Epigenetic inheritance</topic><topic>Epigenetics</topic><topic>Female</topic><topic>Gene Expression Regulation, Neoplastic - drug effects</topic><topic>Genes</topic><topic>Genetic aspects</topic><topic>Ginsenosides - pharmacology</topic><topic>Health aspects</topic><topic>Humans</topic><topic>Medical prognosis</topic><topic>Messenger RNA</topic><topic>Metastasis</topic><topic>Methylation</topic><topic>Methyltransferases</topic><topic>Mortality</topic><topic>MutL Protein Homolog 1 - genetics</topic><topic>Ovarian cancer</topic><topic>Ovarian Neoplasms - drug therapy</topic><topic>Ovarian Neoplasms - genetics</topic><topic>Ovarian Neoplasms - pathology</topic><topic>Physiological aspects</topic><topic>Polymerase chain reaction</topic><topic>Post-translational modifications</topic><topic>RNA</topic><topic>Saponins</topic><topic>Signal Transduction - drug effects</topic><topic>Tumor proteins</topic><topic>Tumor suppressor genes</topic><topic>Tumor Suppressor Protein p53 - genetics</topic><topic>Tumors</topic><topic>Wound care</topic><topic>Wound healing</topic><toplevel>online_resources</toplevel><creatorcontrib>Zhao, Lingqin</creatorcontrib><creatorcontrib>Shou, Huafeng</creatorcontrib><creatorcontrib>Chen, Lu</creatorcontrib><creatorcontrib>Gao, Wen</creatorcontrib><creatorcontrib>Fang, Chenyan</creatorcontrib><creatorcontrib>Zhang, Ping</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>British Nursing Database</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Oncology reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhao, Lingqin</au><au>Shou, Huafeng</au><au>Chen, Lu</au><au>Gao, Wen</au><au>Fang, Chenyan</au><au>Zhang, Ping</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Effects of ginsenoside Rg3 on epigenetic modification in ovarian cancer cells</atitle><jtitle>Oncology reports</jtitle><addtitle>Oncol Rep</addtitle><date>2019-06-01</date><risdate>2019</risdate><volume>41</volume><issue>6</issue><spage>3209</spage><epage>3218</epage><pages>3209-3218</pages><issn>1021-335X</issn><eissn>1791-2431</eissn><abstract>Epigenetic modifications are closely related to oncogene activation and tumor suppressor gene inactivation. The aim of this study was to determine the effects of ginsenoside Rg3 on epigenetic modification in ovarian cancer cells. Cell proliferation, metastasis, invasion and apoptosis were respectively determined using Cell Counting Kit‑8 (CCK‑8), wound healing, Transwell and flow cytometric assays. Methylation levels were determined using methylation specific PCR (MSP). Related‑factor expression was detected by conducting real‑time‑qPCR (RT‑qPCR) and western blotting. The results revealed that cell proliferation was inhibited by ginsenoside Rg3 (0, 25, 50, 100 and 200 µg/ml) in a time‑dependent manner (12, 24 and 48 h). Ginsenoside Rg3 (50, 100 and 200 µg/ml) was selected to treat cells in various experiments. When ovarian cells were treated with ginsenoside Rg3, cell apoptosis was observed to be promoted, while cell metastasis and invasion were inhibited at 48 h. The results of the present study revealed that in the promoter regions of p53, p16 and hMLH1, the methylation levels decreased, while the mRNA and protein levels significantly increased. The activities of DNMTs and mRNA as well as protein levels of DNMT1, DNMT3a and DNMT3b were decreased by Rg3. The data also demonstrated that the mRNA and protein levels of acetyl‑H3 K14/K9 and acetyl‑H4 K12/K5/K16 were increased by Rg3. Hence, ginsenoside Rg3 inhibited ovarian cancer cell viability, migration and invasion as well as promoted cell apoptosis.</abstract><cop>Greece</cop><pub>Spandidos Publications</pub><pmid>31002353</pmid><doi>10.3892/or.2019.7115</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection |
| subjects | Apoptosis Apoptosis - drug effects Cancer cells Cancer metastasis Cancer therapies Care and treatment Cell cycle Cell growth Cell Line, Tumor Cell Proliferation - drug effects Cell Survival - drug effects Cyclin-Dependent Kinase Inhibitor p16 - genetics Deoxyribonucleic acid DNA DNA (Cytosine-5-)-Methyltransferase 1 - genetics DNA (Cytosine-5-)-Methyltransferases - genetics DNA methylation DNA Methylation - genetics DNA Methyltransferase 3A DNA Methyltransferase 3B Dosage and administration Epigenesis, Genetic Epigenetic inheritance Epigenetics Female Gene Expression Regulation, Neoplastic - drug effects Genes Genetic aspects Ginsenosides - pharmacology Health aspects Humans Medical prognosis Messenger RNA Metastasis Methylation Methyltransferases Mortality MutL Protein Homolog 1 - genetics Ovarian cancer Ovarian Neoplasms - drug therapy Ovarian Neoplasms - genetics Ovarian Neoplasms - pathology Physiological aspects Polymerase chain reaction Post-translational modifications RNA Saponins Signal Transduction - drug effects Tumor proteins Tumor suppressor genes Tumor Suppressor Protein p53 - genetics Tumors Wound care Wound healing |
| title | Effects of ginsenoside Rg3 on epigenetic modification in ovarian cancer cells |
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