Apoptotic Death of Prostate Cancer Cells by a Gonadotropin-Releasing Hormone-II Antagonist
DC Field | Value | Language |
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dc.contributor.author | Park, Sumi | - |
dc.contributor.author | Han, Ji Man | - |
dc.contributor.author | Cheon, Jun | - |
dc.contributor.author | Hwang, Jong-Ik | - |
dc.contributor.author | Seong, Jae Young | - |
dc.date.accessioned | 2021-09-05T07:53:48Z | - |
dc.date.available | 2021-09-05T07:53:48Z | - |
dc.date.created | 2021-06-15 | - |
dc.date.issued | 2014-06-13 | - |
dc.identifier.issn | 1932-6203 | - |
dc.identifier.uri | https://scholar.korea.ac.kr/handle/2021.sw.korea/98235 | - |
dc.description.abstract | Gonadotropin-releasing hormone-I (GnRH-I) has attracted strong attention as a hormonal therapeutic tool, particularly for androgen-dependent prostate cancer patients. However, the androgen-independency of the cancer in advanced stages has spurred researchers to look for new medical treatments. In previous reports, we developed the GnRH-II antagonist Trp-1 to inhibit proliferation and stimulate the autophagic death of various prostate cancer cells, including androgen-independent cells. We further screened many GnRH-II antagonists to identify molecules with higher efficiency. Here, we investigated the effect of SN09-2 on the growth of PC3 prostate cancer cells. SN09-2 reduced the growth of prostate cancer cells but had no effect on cells derived from other tissues. Compared with Trp-1, SN09-2 conspicuously inhibited prostate cancer cell growth, even at low concentrations. SN09-2-induced PC3 cell growth inhibition was associated with decreased membrane potential in mitochondria where the antagonist was accumulated, and increased mitochondrial and cytosolic reactive oxygen species. SN09-2 induced lactate dehydrogenase release into the media and annexin V-staining on the PC3 cell surface, suggesting that the antagonist stimulated prostate cancer cell death by activating apoptotic signaling pathways. Furthermore, cytochrome c release from mitochondria to the cytosol and caspase-3 activation occurred in a concentration-and time-dependent manner. SN09-2 also inhibited the growth of PC3 cells xenotransplanted into nude mice. These results demonstrate that SN09-2 directly induces mitochondrial dysfunction and the consequent ROS generation, leading to not only growth inhibition but also apoptosis of prostate cancer cells. | - |
dc.language | English | - |
dc.language.iso | en | - |
dc.publisher | PUBLIC LIBRARY SCIENCE | - |
dc.subject | GNRH-II | - |
dc.subject | LUTEINIZING-HORMONE | - |
dc.subject | MITOCHONDRIAL HOMEOSTASIS | - |
dc.subject | GROWTH-FACTOR | - |
dc.subject | RECEPTOR | - |
dc.subject | AUTOPHAGY | - |
dc.subject | PITUITARY | - |
dc.subject | (GNRH)-I | - |
dc.subject | PATHWAY | - |
dc.subject | KINASE | - |
dc.title | Apoptotic Death of Prostate Cancer Cells by a Gonadotropin-Releasing Hormone-II Antagonist | - |
dc.type | Article | - |
dc.contributor.affiliatedAuthor | Cheon, Jun | - |
dc.contributor.affiliatedAuthor | Hwang, Jong-Ik | - |
dc.contributor.affiliatedAuthor | Seong, Jae Young | - |
dc.identifier.doi | 10.1371/journal.pone.0099723 | - |
dc.identifier.scopusid | 2-s2.0-84903119934 | - |
dc.identifier.wosid | 000338278100073 | - |
dc.identifier.bibliographicCitation | PLOS ONE, v.9, no.6 | - |
dc.relation.isPartOf | PLOS ONE | - |
dc.citation.title | PLOS ONE | - |
dc.citation.volume | 9 | - |
dc.citation.number | 6 | - |
dc.type.rims | ART | - |
dc.type.docType | Article | - |
dc.description.journalClass | 1 | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.relation.journalResearchArea | Science & Technology - Other Topics | - |
dc.relation.journalWebOfScienceCategory | Multidisciplinary Sciences | - |
dc.subject.keywordPlus | GNRH-II | - |
dc.subject.keywordPlus | LUTEINIZING-HORMONE | - |
dc.subject.keywordPlus | MITOCHONDRIAL HOMEOSTASIS | - |
dc.subject.keywordPlus | GROWTH-FACTOR | - |
dc.subject.keywordPlus | RECEPTOR | - |
dc.subject.keywordPlus | AUTOPHAGY | - |
dc.subject.keywordPlus | PITUITARY | - |
dc.subject.keywordPlus | (GNRH)-I | - |
dc.subject.keywordPlus | PATHWAY | - |
dc.subject.keywordPlus | KINASE | - |
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