3-Hydroxyterphenyllin, a natural fungal metabolite, induces apoptosis and S phase arrest in human ovarian carcinoma cells
In the present study, we evaluated 3-Hydroxyter-phenyllin (3-HT) as a potential anticancer agent using the human ovarian cancer cells A2780/CP70 and OVCAR-3, and normal human epithelial ovarian cells IOSE-364 as an in vitro model. 3-HT suppressed proliferation and caused cytotoxicity against A2780/C...
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| Veröffentlicht in: | International journal of oncology 2017-04, Vol.50 (4), p.1392-1402 |
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| creator | Wang, Yaomin Compton, Casey Rankin, Gary O Cutler, Stephen J Rojanasakul, Yon Tu, Youying Chen, Yi Charlie |
| description | In the present study, we evaluated 3-Hydroxyter-phenyllin (3-HT) as a potential anticancer agent using the human ovarian cancer cells A2780/CP70 and OVCAR-3, and normal human epithelial ovarian cells IOSE-364 as an in vitro model. 3-HT suppressed proliferation and caused cytotoxicity against A2780/CP70 and OVCAR-3 cells, while it exhibited lower cytotoxicity in IOSE-364 cells. Subsequently, we found that 3-HT induced S phase arrest and apoptosis in a dose-independent manner. Further investigation revealed that S phase arrest was related with DNA damage which mediated the ATM/p53/Chk2 pathway. Downregulation of cyclin D1, cyclin A2, cyclin E1, CDK2, CDK4 and Cdc25C, and the upregulation of Cdc25A and cyclin B1 led to the accumulation of cells in S phase. The apoptotic effect was confirmed by Hoechst 33342 staining, depolarization of mitochondrial membrane potential and activation of cleaved caspase-3 and PARP1. Additional results revealed both intrinsic and extrinsic apoptotic pathways were involved. The intrinsic apoptotic pathway was activated through decreasing the protein levels of Bcl2, Bcl-xL and procaspase-9 and increasing the protein level of Puma. The induction of DR5 and DR4 indicated that the extrinsic apoptotic pathway was also activated. Induction of ROS and activation of ERK were observed in ovarian cancer cells. We therefore concluded that 3-HT possessed anti-proliferative effect on A2780/CP70 and OVCAR-3 cells, induced S phase arrest and caused apoptosis. Taken together, we propose that 3-HT shows promise as a therapeutic candidate for treating ovarian cancer. |
| doi_str_mv | 10.3892/ijo.2017.3894 |
| format | Article |
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Subsequently, we found that 3-HT induced S phase arrest and apoptosis in a dose-independent manner. Further investigation revealed that S phase arrest was related with DNA damage which mediated the ATM/p53/Chk2 pathway. Downregulation of cyclin D1, cyclin A2, cyclin E1, CDK2, CDK4 and Cdc25C, and the upregulation of Cdc25A and cyclin B1 led to the accumulation of cells in S phase. The apoptotic effect was confirmed by Hoechst 33342 staining, depolarization of mitochondrial membrane potential and activation of cleaved caspase-3 and PARP1. Additional results revealed both intrinsic and extrinsic apoptotic pathways were involved. The intrinsic apoptotic pathway was activated through decreasing the protein levels of Bcl2, Bcl-xL and procaspase-9 and increasing the protein level of Puma. The induction of DR5 and DR4 indicated that the extrinsic apoptotic pathway was also activated. Induction of ROS and activation of ERK were observed in ovarian cancer cells. We therefore concluded that 3-HT possessed anti-proliferative effect on A2780/CP70 and OVCAR-3 cells, induced S phase arrest and caused apoptosis. Taken together, we propose that 3-HT shows promise as a therapeutic candidate for treating ovarian cancer.</description><identifier>ISSN: 1019-6439</identifier><identifier>EISSN: 1791-2423</identifier><identifier>DOI: 10.3892/ijo.2017.3894</identifier><identifier>PMID: 28259974</identifier><language>eng</language><publisher>Greece: Spandidos Publications</publisher><subject>Antineoplastic Agents - therapeutic use ; Apoptosis ; Apoptosis - drug effects ; Aspergillus - chemistry ; Ataxia Telangiectasia Mutated Proteins - metabolism ; Cancer therapies ; Care and treatment ; Cell culture ; Cell cycle ; Cell Cycle Proteins - metabolism ; Cell growth ; Cell Line, Transformed ; Cell Line, Tumor ; Checkpoint Kinase 2 - metabolism ; Cytotoxicity ; Deoxyribonucleic acid ; Development and progression ; DNA ; DNA Damage - drug effects ; Epithelial Cells ; Female ; Genetic aspects ; Genetic regulation ; Health aspects ; Humans ; Immunoglobulins ; Kinases ; Membrane Potential, Mitochondrial - drug effects ; Metabolites ; Natural products ; Ovarian cancer ; Ovarian Neoplasms - drug therapy ; Ovary - cytology ; Poly (ADP-Ribose) Polymerase-1 - metabolism ; Prostate ; Proteins ; Rodents ; S Phase Cell Cycle Checkpoints - drug effects ; Signal Transduction ; Studies ; Terphenyl Compounds - therapeutic use ; Tumor necrosis factor-TNF ; Tumor Suppressor Protein p53 - metabolism</subject><ispartof>International journal of oncology, 2017-04, Vol.50 (4), p.1392-1402</ispartof><rights>COPYRIGHT 2017 Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2017</rights><rights>Copyright © 2017, Spandidos Publications 2017</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c513t-226c002f6a5d3c10714d5f0005b241a52feab230cad6f66290d5bfb27e34431a3</citedby><cites>FETCH-LOGICAL-c513t-226c002f6a5d3c10714d5f0005b241a52feab230cad6f66290d5bfb27e34431a3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,776,780,881,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28259974$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wang, Yaomin</creatorcontrib><creatorcontrib>Compton, Casey</creatorcontrib><creatorcontrib>Rankin, Gary O</creatorcontrib><creatorcontrib>Cutler, Stephen J</creatorcontrib><creatorcontrib>Rojanasakul, Yon</creatorcontrib><creatorcontrib>Tu, Youying</creatorcontrib><creatorcontrib>Chen, Yi Charlie</creatorcontrib><title>3-Hydroxyterphenyllin, a natural fungal metabolite, induces apoptosis and S phase arrest in human ovarian carcinoma cells</title><title>International journal of oncology</title><addtitle>Int J Oncol</addtitle><description>In the present study, we evaluated 3-Hydroxyter-phenyllin (3-HT) as a potential anticancer agent using the human ovarian cancer cells A2780/CP70 and OVCAR-3, and normal human epithelial ovarian cells IOSE-364 as an in vitro model. 3-HT suppressed proliferation and caused cytotoxicity against A2780/CP70 and OVCAR-3 cells, while it exhibited lower cytotoxicity in IOSE-364 cells. Subsequently, we found that 3-HT induced S phase arrest and apoptosis in a dose-independent manner. Further investigation revealed that S phase arrest was related with DNA damage which mediated the ATM/p53/Chk2 pathway. Downregulation of cyclin D1, cyclin A2, cyclin E1, CDK2, CDK4 and Cdc25C, and the upregulation of Cdc25A and cyclin B1 led to the accumulation of cells in S phase. The apoptotic effect was confirmed by Hoechst 33342 staining, depolarization of mitochondrial membrane potential and activation of cleaved caspase-3 and PARP1. Additional results revealed both intrinsic and extrinsic apoptotic pathways were involved. The intrinsic apoptotic pathway was activated through decreasing the protein levels of Bcl2, Bcl-xL and procaspase-9 and increasing the protein level of Puma. The induction of DR5 and DR4 indicated that the extrinsic apoptotic pathway was also activated. Induction of ROS and activation of ERK were observed in ovarian cancer cells. We therefore concluded that 3-HT possessed anti-proliferative effect on A2780/CP70 and OVCAR-3 cells, induced S phase arrest and caused apoptosis. Taken together, we propose that 3-HT shows promise as a therapeutic candidate for treating ovarian cancer.</description><subject>Antineoplastic Agents - therapeutic use</subject><subject>Apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>Aspergillus - chemistry</subject><subject>Ataxia Telangiectasia Mutated Proteins - metabolism</subject><subject>Cancer therapies</subject><subject>Care and treatment</subject><subject>Cell culture</subject><subject>Cell cycle</subject><subject>Cell Cycle Proteins - metabolism</subject><subject>Cell growth</subject><subject>Cell Line, Transformed</subject><subject>Cell Line, Tumor</subject><subject>Checkpoint Kinase 2 - metabolism</subject><subject>Cytotoxicity</subject><subject>Deoxyribonucleic acid</subject><subject>Development and progression</subject><subject>DNA</subject><subject>DNA Damage - drug effects</subject><subject>Epithelial Cells</subject><subject>Female</subject><subject>Genetic aspects</subject><subject>Genetic regulation</subject><subject>Health aspects</subject><subject>Humans</subject><subject>Immunoglobulins</subject><subject>Kinases</subject><subject>Membrane Potential, Mitochondrial - drug effects</subject><subject>Metabolites</subject><subject>Natural products</subject><subject>Ovarian cancer</subject><subject>Ovarian Neoplasms - drug therapy</subject><subject>Ovary - cytology</subject><subject>Poly (ADP-Ribose) Polymerase-1 - metabolism</subject><subject>Prostate</subject><subject>Proteins</subject><subject>Rodents</subject><subject>S Phase Cell Cycle Checkpoints - drug effects</subject><subject>Signal Transduction</subject><subject>Studies</subject><subject>Terphenyl Compounds - therapeutic use</subject><subject>Tumor necrosis factor-TNF</subject><subject>Tumor Suppressor Protein p53 - metabolism</subject><issn>1019-6439</issn><issn>1791-2423</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNptks9rFTEQxxdRbK0evUpA8NR95ufuy0UoRa1Q8KCew2w26eaxm6xJtnT_e7O01j6QHCaTfObLzPCtqrcE79he0o_uEHYUk3bL-LPqlLSS1JRT9rzcMZF1w5k8qV6ldMCYCoHJy-qE7qmQsuWn1crqq7WP4W7NJs6D8es4On-OAHnIS4QR2cXflDCZDF0YXTbnyPl-0SYhmMOcQ3Ll5nv0A80DJIMgRpNygdCwTOBRuIXoStQQtfNhAqTNOKbX1QsLYzJvHuJZ9evL55-XV_X196_fLi-uay0IyzWljS6N2wZEzzTBLeG9sBhj0VFOQFBroKMMa-gb2zRU4l50tqOtYZwzAuys-nSvOy_dZHptfC5jqTm6CeKqAjh1_OPdoG7CrRKsYfuWF4H3DwIx_F7KaOoQluhLz4pI0TaCSkL-UWVZRjlvQxHTk0taXfACiJawTWv3H6qc3kxOB2-sK-9HBR-eFAwGxjykMC7ZBZ-Owfoe1DGkFI19nJBgtTlFFaeozSlbtvHvnq7lkf5rDfYHN6O5ww</recordid><startdate>20170401</startdate><enddate>20170401</enddate><creator>Wang, Yaomin</creator><creator>Compton, Casey</creator><creator>Rankin, Gary O</creator><creator>Cutler, Stephen J</creator><creator>Rojanasakul, Yon</creator><creator>Tu, Youying</creator><creator>Chen, Yi Charlie</creator><general>Spandidos Publications</general><general>Spandidos Publications UK Ltd</general><general>D.A. 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Subsequently, we found that 3-HT induced S phase arrest and apoptosis in a dose-independent manner. Further investigation revealed that S phase arrest was related with DNA damage which mediated the ATM/p53/Chk2 pathway. Downregulation of cyclin D1, cyclin A2, cyclin E1, CDK2, CDK4 and Cdc25C, and the upregulation of Cdc25A and cyclin B1 led to the accumulation of cells in S phase. The apoptotic effect was confirmed by Hoechst 33342 staining, depolarization of mitochondrial membrane potential and activation of cleaved caspase-3 and PARP1. Additional results revealed both intrinsic and extrinsic apoptotic pathways were involved. The intrinsic apoptotic pathway was activated through decreasing the protein levels of Bcl2, Bcl-xL and procaspase-9 and increasing the protein level of Puma. The induction of DR5 and DR4 indicated that the extrinsic apoptotic pathway was also activated. Induction of ROS and activation of ERK were observed in ovarian cancer cells. We therefore concluded that 3-HT possessed anti-proliferative effect on A2780/CP70 and OVCAR-3 cells, induced S phase arrest and caused apoptosis. Taken together, we propose that 3-HT shows promise as a therapeutic candidate for treating ovarian cancer.</abstract><cop>Greece</cop><pub>Spandidos Publications</pub><pmid>28259974</pmid><doi>10.3892/ijo.2017.3894</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Antineoplastic Agents - therapeutic use Apoptosis Apoptosis - drug effects Aspergillus - chemistry Ataxia Telangiectasia Mutated Proteins - metabolism Cancer therapies Care and treatment Cell culture Cell cycle Cell Cycle Proteins - metabolism Cell growth Cell Line, Transformed Cell Line, Tumor Checkpoint Kinase 2 - metabolism Cytotoxicity Deoxyribonucleic acid Development and progression DNA DNA Damage - drug effects Epithelial Cells Female Genetic aspects Genetic regulation Health aspects Humans Immunoglobulins Kinases Membrane Potential, Mitochondrial - drug effects Metabolites Natural products Ovarian cancer Ovarian Neoplasms - drug therapy Ovary - cytology Poly (ADP-Ribose) Polymerase-1 - metabolism Prostate Proteins Rodents S Phase Cell Cycle Checkpoints - drug effects Signal Transduction Studies Terphenyl Compounds - therapeutic use Tumor necrosis factor-TNF Tumor Suppressor Protein p53 - metabolism |
| title | 3-Hydroxyterphenyllin, a natural fungal metabolite, induces apoptosis and S phase arrest in human ovarian carcinoma cells |
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