Trichodermin Induces G0/G1 Cell Cycle Arrest by Inhibiting c-Myc in Ovarian Cancer Cells and Tumor Xenograft-Bearing Mice
Ovarian cancer is a fatal gynecological cancer because of a lack of early diagnosis, which often relapses as chemoresistant. Trichodermin, a trichothecene first isolated from , is an inhibitor of eukaryotic protein synthesis. However, whether trichodermin is able to suppress ovarian cancer or not wa...
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| Veröffentlicht in: | International journal of molecular sciences 2021-05, Vol.22 (9), p.5022 |
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| creator | Gao, Ying Miles, Sarah L Dasgupta, Piyali Rankin, Gary O Cutler, Stephen Chen, Yi Charlie |
| description | Ovarian cancer is a fatal gynecological cancer because of a lack of early diagnosis, which often relapses as chemoresistant. Trichodermin, a trichothecene first isolated from
, is an inhibitor of eukaryotic protein synthesis. However, whether trichodermin is able to suppress ovarian cancer or not was unclear. In this study, trichodermin (0.5 µM or greater) significantly decreased the proliferation of two ovarian cancer cell lines A2780/CP70 and OVCAR-3. Normal ovarian IOSE 346 cells were much less susceptible to trichodermin than the cancer cell lines. Trichodermin predominantly inhibited ovarian cancer cells by inducing G0/G1 cell cycle arrest rather than apoptosis. Trichodermin decreased the expression of cyclin D1, CDK4, CDK2, retinoblastoma protein, Cdc25A, and c-Myc but showed little effect on the expression of p21
, p27
, or p16
. c-Myc was a key target of trichodermin. Trichodermin regulated the expression of Cdc25A and its downstream proteins via c-Myc. Overexpression of c-Myc attenuated trichodermin's anti-ovarian cancer activity. In addition, trichodermin decelerated tumor growth in BALB/c nude mice, proving its effectiveness in vivo. These findings suggested that trichodermin has the potential to contribute to the treatment of ovarian cancer. |
| doi_str_mv | 10.3390/ijms22095022 |
| format | Article |
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, is an inhibitor of eukaryotic protein synthesis. However, whether trichodermin is able to suppress ovarian cancer or not was unclear. In this study, trichodermin (0.5 µM or greater) significantly decreased the proliferation of two ovarian cancer cell lines A2780/CP70 and OVCAR-3. Normal ovarian IOSE 346 cells were much less susceptible to trichodermin than the cancer cell lines. Trichodermin predominantly inhibited ovarian cancer cells by inducing G0/G1 cell cycle arrest rather than apoptosis. Trichodermin decreased the expression of cyclin D1, CDK4, CDK2, retinoblastoma protein, Cdc25A, and c-Myc but showed little effect on the expression of p21
, p27
, or p16
. c-Myc was a key target of trichodermin. Trichodermin regulated the expression of Cdc25A and its downstream proteins via c-Myc. Overexpression of c-Myc attenuated trichodermin's anti-ovarian cancer activity. In addition, trichodermin decelerated tumor growth in BALB/c nude mice, proving its effectiveness in vivo. These findings suggested that trichodermin has the potential to contribute to the treatment of ovarian cancer.</description><identifier>ISSN: 1422-0067</identifier><identifier>ISSN: 1661-6596</identifier><identifier>EISSN: 1422-0067</identifier><identifier>DOI: 10.3390/ijms22095022</identifier><identifier>PMID: 34065149</identifier><language>eng</language><publisher>Switzerland: MDPI AG</publisher><subject>Animals ; Antibodies ; Apoptosis ; Biomarkers, Tumor ; c-Myc protein ; Cancer therapies ; Cell cycle ; Cell Cycle - drug effects ; Cell growth ; Cell Line, Tumor ; Cell Proliferation - drug effects ; Cell Survival - drug effects ; Chemotherapy ; Cyclin D1 ; Cyclin-dependent kinase 2 ; Cyclin-dependent kinase 4 ; Cyclin-dependent kinase inhibitor p21 ; Cyclin-dependent kinase inhibitor p27 ; Cyclin-dependent kinases ; Cyclin-Dependent Kinases - metabolism ; Deceleration ; Disease Models, Animal ; Drugs ; Experiments ; FDA approval ; Female ; Flow cytometry ; Fungi ; G1 Phase Cell Cycle Checkpoints - drug effects ; Gene Expression Regulation, Neoplastic - drug effects ; Genes, myc ; Gynecological cancer ; Humans ; INK4a protein ; Kinases ; Mice ; Myc protein ; Ovarian cancer ; Ovarian Neoplasms ; p16 Protein ; Protein biosynthesis ; Protein synthesis ; Proteins ; Retina ; Retinoblastoma ; Retinoblastoma protein ; Software ; Trichodermin - chemistry ; Trichodermin - pharmacology ; Tumor cell lines ; Tumors ; Variance analysis ; Xenograft Model Antitumor Assays ; Xenografts ; Xenotransplantation</subject><ispartof>International journal of molecular sciences, 2021-05, Vol.22 (9), p.5022</ispartof><rights>2021 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2021 by the authors. 2021</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c412t-d80d4ab53ce1fc5e99a55a5ebec875c76f65aa5ade82d762b864ab337a2790f13</citedby><cites>FETCH-LOGICAL-c412t-d80d4ab53ce1fc5e99a55a5ebec875c76f65aa5ade82d762b864ab337a2790f13</cites><orcidid>0000-0001-6865-9512 ; 0000-0003-0696-7880 ; 0000-0002-5385-3512 ; 0000-0002-7997-2309</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8126000/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8126000/$$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/34065149$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Gao, Ying</creatorcontrib><creatorcontrib>Miles, Sarah L</creatorcontrib><creatorcontrib>Dasgupta, Piyali</creatorcontrib><creatorcontrib>Rankin, Gary O</creatorcontrib><creatorcontrib>Cutler, Stephen</creatorcontrib><creatorcontrib>Chen, Yi Charlie</creatorcontrib><title>Trichodermin Induces G0/G1 Cell Cycle Arrest by Inhibiting c-Myc in Ovarian Cancer Cells and Tumor Xenograft-Bearing Mice</title><title>International journal of molecular sciences</title><addtitle>Int J Mol Sci</addtitle><description>Ovarian cancer is a fatal gynecological cancer because of a lack of early diagnosis, which often relapses as chemoresistant. Trichodermin, a trichothecene first isolated from
, is an inhibitor of eukaryotic protein synthesis. However, whether trichodermin is able to suppress ovarian cancer or not was unclear. In this study, trichodermin (0.5 µM or greater) significantly decreased the proliferation of two ovarian cancer cell lines A2780/CP70 and OVCAR-3. Normal ovarian IOSE 346 cells were much less susceptible to trichodermin than the cancer cell lines. Trichodermin predominantly inhibited ovarian cancer cells by inducing G0/G1 cell cycle arrest rather than apoptosis. Trichodermin decreased the expression of cyclin D1, CDK4, CDK2, retinoblastoma protein, Cdc25A, and c-Myc but showed little effect on the expression of p21
, p27
, or p16
. c-Myc was a key target of trichodermin. Trichodermin regulated the expression of Cdc25A and its downstream proteins via c-Myc. Overexpression of c-Myc attenuated trichodermin's anti-ovarian cancer activity. In addition, trichodermin decelerated tumor growth in BALB/c nude mice, proving its effectiveness in vivo. These findings suggested that trichodermin has the potential to contribute to the treatment of ovarian cancer.</description><subject>Animals</subject><subject>Antibodies</subject><subject>Apoptosis</subject><subject>Biomarkers, Tumor</subject><subject>c-Myc protein</subject><subject>Cancer therapies</subject><subject>Cell cycle</subject><subject>Cell Cycle - drug effects</subject><subject>Cell growth</subject><subject>Cell Line, Tumor</subject><subject>Cell Proliferation - drug effects</subject><subject>Cell Survival - drug effects</subject><subject>Chemotherapy</subject><subject>Cyclin D1</subject><subject>Cyclin-dependent kinase 2</subject><subject>Cyclin-dependent kinase 4</subject><subject>Cyclin-dependent kinase inhibitor p21</subject><subject>Cyclin-dependent kinase inhibitor p27</subject><subject>Cyclin-dependent kinases</subject><subject>Cyclin-Dependent Kinases - metabolism</subject><subject>Deceleration</subject><subject>Disease Models, Animal</subject><subject>Drugs</subject><subject>Experiments</subject><subject>FDA approval</subject><subject>Female</subject><subject>Flow cytometry</subject><subject>Fungi</subject><subject>G1 Phase Cell Cycle Checkpoints - drug effects</subject><subject>Gene Expression Regulation, Neoplastic - drug effects</subject><subject>Genes, myc</subject><subject>Gynecological cancer</subject><subject>Humans</subject><subject>INK4a protein</subject><subject>Kinases</subject><subject>Mice</subject><subject>Myc protein</subject><subject>Ovarian cancer</subject><subject>Ovarian Neoplasms</subject><subject>p16 Protein</subject><subject>Protein biosynthesis</subject><subject>Protein synthesis</subject><subject>Proteins</subject><subject>Retina</subject><subject>Retinoblastoma</subject><subject>Retinoblastoma protein</subject><subject>Software</subject><subject>Trichodermin - chemistry</subject><subject>Trichodermin - pharmacology</subject><subject>Tumor cell lines</subject><subject>Tumors</subject><subject>Variance analysis</subject><subject>Xenograft Model Antitumor Assays</subject><subject>Xenografts</subject><subject>Xenotransplantation</subject><issn>1422-0067</issn><issn>1661-6596</issn><issn>1422-0067</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNpdkUFv1DAQhS0EoqVw44wsceFA6NiOneSCVCJYKrXqZZG4WY4z2fUqsYudVMq_x6WlWjh5JH_vad48Qt4y-CREA-fuMCXOoZHA-TNyykrOCwBVPT-aT8irlA4AXHDZvCQnogQlWdmcknUbnd2HHuPkPL30_WIx0Q2cbxhtcRxpu9oR6UWMmGbarRnZu87Nzu-oLa5XS7Ps5s5EZzxtjbcY_-gSNb6n22UKkf5EH3bRDHPxBTOYldfO4mvyYjBjwjeP7xn58e3rtv1eXN1sLtuLq8KWjM9FX0Nfmk4Ki2ywEpvGSGkkdmjrStpKDUoaI02PNe8rxbtaZVyIyvCqgYGJM_L5wfd26SbsLfo5mlHfRjeZuOpgnP73x7u93oU7XTOuACAbfHg0iOHXks-gJ5dszmg8hiVpLoUqG5C8zOj7_9BDWKLP8TLF6-zH1D318YGyMaQUcXhahoG-71Qfd5rxd8cBnuC_JYrfKIKdWw</recordid><startdate>20210509</startdate><enddate>20210509</enddate><creator>Gao, Ying</creator><creator>Miles, Sarah L</creator><creator>Dasgupta, Piyali</creator><creator>Rankin, Gary O</creator><creator>Cutler, Stephen</creator><creator>Chen, Yi Charlie</creator><general>MDPI AG</general><general>MDPI</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>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>PHGZM</scope><scope>PHGZT</scope><scope>PIMPY</scope><scope>PJZUB</scope><scope>PKEHL</scope><scope>PPXIY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0001-6865-9512</orcidid><orcidid>https://orcid.org/0000-0003-0696-7880</orcidid><orcidid>https://orcid.org/0000-0002-5385-3512</orcidid><orcidid>https://orcid.org/0000-0002-7997-2309</orcidid></search><sort><creationdate>20210509</creationdate><title>Trichodermin Induces G0/G1 Cell Cycle Arrest by Inhibiting c-Myc in Ovarian Cancer Cells and Tumor Xenograft-Bearing Mice</title><author>Gao, Ying ; Miles, Sarah L ; Dasgupta, Piyali ; Rankin, Gary O ; Cutler, Stephen ; Chen, Yi Charlie</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c412t-d80d4ab53ce1fc5e99a55a5ebec875c76f65aa5ade82d762b864ab337a2790f13</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Animals</topic><topic>Antibodies</topic><topic>Apoptosis</topic><topic>Biomarkers, Tumor</topic><topic>c-Myc protein</topic><topic>Cancer therapies</topic><topic>Cell cycle</topic><topic>Cell Cycle - drug effects</topic><topic>Cell growth</topic><topic>Cell Line, Tumor</topic><topic>Cell Proliferation - drug effects</topic><topic>Cell Survival - drug effects</topic><topic>Chemotherapy</topic><topic>Cyclin D1</topic><topic>Cyclin-dependent kinase 2</topic><topic>Cyclin-dependent kinase 4</topic><topic>Cyclin-dependent kinase inhibitor p21</topic><topic>Cyclin-dependent kinase inhibitor p27</topic><topic>Cyclin-dependent kinases</topic><topic>Cyclin-Dependent Kinases - metabolism</topic><topic>Deceleration</topic><topic>Disease Models, Animal</topic><topic>Drugs</topic><topic>Experiments</topic><topic>FDA approval</topic><topic>Female</topic><topic>Flow cytometry</topic><topic>Fungi</topic><topic>G1 Phase Cell Cycle Checkpoints - drug effects</topic><topic>Gene Expression Regulation, Neoplastic - drug effects</topic><topic>Genes, myc</topic><topic>Gynecological cancer</topic><topic>Humans</topic><topic>INK4a protein</topic><topic>Kinases</topic><topic>Mice</topic><topic>Myc protein</topic><topic>Ovarian cancer</topic><topic>Ovarian Neoplasms</topic><topic>p16 Protein</topic><topic>Protein biosynthesis</topic><topic>Protein synthesis</topic><topic>Proteins</topic><topic>Retina</topic><topic>Retinoblastoma</topic><topic>Retinoblastoma protein</topic><topic>Software</topic><topic>Trichodermin - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>International journal of molecular sciences</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Gao, Ying</au><au>Miles, Sarah L</au><au>Dasgupta, Piyali</au><au>Rankin, Gary O</au><au>Cutler, Stephen</au><au>Chen, Yi Charlie</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Trichodermin Induces G0/G1 Cell Cycle Arrest by Inhibiting c-Myc in Ovarian Cancer Cells and Tumor Xenograft-Bearing Mice</atitle><jtitle>International journal of molecular sciences</jtitle><addtitle>Int J Mol Sci</addtitle><date>2021-05-09</date><risdate>2021</risdate><volume>22</volume><issue>9</issue><spage>5022</spage><pages>5022-</pages><issn>1422-0067</issn><issn>1661-6596</issn><eissn>1422-0067</eissn><abstract>Ovarian cancer is a fatal gynecological cancer because of a lack of early diagnosis, which often relapses as chemoresistant. Trichodermin, a trichothecene first isolated from
, is an inhibitor of eukaryotic protein synthesis. However, whether trichodermin is able to suppress ovarian cancer or not was unclear. In this study, trichodermin (0.5 µM or greater) significantly decreased the proliferation of two ovarian cancer cell lines A2780/CP70 and OVCAR-3. Normal ovarian IOSE 346 cells were much less susceptible to trichodermin than the cancer cell lines. Trichodermin predominantly inhibited ovarian cancer cells by inducing G0/G1 cell cycle arrest rather than apoptosis. Trichodermin decreased the expression of cyclin D1, CDK4, CDK2, retinoblastoma protein, Cdc25A, and c-Myc but showed little effect on the expression of p21
, p27
, or p16
. c-Myc was a key target of trichodermin. Trichodermin regulated the expression of Cdc25A and its downstream proteins via c-Myc. Overexpression of c-Myc attenuated trichodermin's anti-ovarian cancer activity. In addition, trichodermin decelerated tumor growth in BALB/c nude mice, proving its effectiveness in vivo. These findings suggested that trichodermin has the potential to contribute to the treatment of ovarian cancer.</abstract><cop>Switzerland</cop><pub>MDPI AG</pub><pmid>34065149</pmid><doi>10.3390/ijms22095022</doi><orcidid>https://orcid.org/0000-0001-6865-9512</orcidid><orcidid>https://orcid.org/0000-0003-0696-7880</orcidid><orcidid>https://orcid.org/0000-0002-5385-3512</orcidid><orcidid>https://orcid.org/0000-0002-7997-2309</orcidid><oa>free_for_read</oa></addata></record> |
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| ispartof | International journal of molecular sciences, 2021-05, Vol.22 (9), p.5022 |
| issn | 1422-0067 1661-6596 1422-0067 |
| language | eng |
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| source | MDPI - Multidisciplinary Digital Publishing Institute; MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central |
| subjects | Animals Antibodies Apoptosis Biomarkers, Tumor c-Myc protein Cancer therapies Cell cycle Cell Cycle - drug effects Cell growth Cell Line, Tumor Cell Proliferation - drug effects Cell Survival - drug effects Chemotherapy Cyclin D1 Cyclin-dependent kinase 2 Cyclin-dependent kinase 4 Cyclin-dependent kinase inhibitor p21 Cyclin-dependent kinase inhibitor p27 Cyclin-dependent kinases Cyclin-Dependent Kinases - metabolism Deceleration Disease Models, Animal Drugs Experiments FDA approval Female Flow cytometry Fungi G1 Phase Cell Cycle Checkpoints - drug effects Gene Expression Regulation, Neoplastic - drug effects Genes, myc Gynecological cancer Humans INK4a protein Kinases Mice Myc protein Ovarian cancer Ovarian Neoplasms p16 Protein Protein biosynthesis Protein synthesis Proteins Retina Retinoblastoma Retinoblastoma protein Software Trichodermin - chemistry Trichodermin - pharmacology Tumor cell lines Tumors Variance analysis Xenograft Model Antitumor Assays Xenografts Xenotransplantation |
| title | Trichodermin Induces G0/G1 Cell Cycle Arrest by Inhibiting c-Myc in Ovarian Cancer Cells and Tumor Xenograft-Bearing Mice |
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