A novel antitumor piperazine alkyl compound causes apoptosis by inducing RhoB expression via ROS-mediated c-Abl/p38 MAPK signaling

Cited 21 time in scopus
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dc.contributor.authorKyung-Sook Chung-
dc.contributor.authorG Han-
dc.contributor.authorBo Kyung Kim-
dc.contributor.authorH M Kim-
dc.contributor.authorJ S Yang-
dc.contributor.authorJiwon Ahn-
dc.contributor.authorK Lee-
dc.contributor.authorK B Song-
dc.contributor.authorMi Sun Won-
dc.date.accessioned2017-04-19T09:47:33Z-
dc.date.available2017-04-19T09:47:33Z-
dc.date.issued2013-
dc.identifier.issn0344-5704-
dc.identifier.uri10.1007/s00280-013-2310-yko
dc.identifier.urihttps://oak.kribb.re.kr/handle/201005/11699-
dc.description.abstractPurpose: We investigated the action mechanism of a novel anticancer compound, KR28 (1-allyl-4-dodecanoyl-1-ethyl-piperazin-1-ium; bromide), to induce apoptosis of human prostate carcinoma PC-3 cells. Methods: To explore an apoptotic signaling of KR28, we used ROS assay, SRB assay, flow cytometry analysis, reporter assay, xenograft assay, Western blotting, and RT-PCR analysis. Results: The growth inhibitory action of KR28 is cell line specific, impeding the growth of prostate carcinoma PC-3 and stomach carcinoma NUGC-3 cells. KR28 showed strong antitumor activity in PC-3 mouse xenograft model. KR28 increased ROS production, leading to nuclear c-Abl expression, which in turn activated p38 mitogen-activated protein kinase (MAPK) to enhance the expression of RhoB, an apoptosis inducer. The KR28-induced apoptosis was abrogated by the ROS scavenger N-acetylcysteine and by knockdown of c-Abl, p38 MAPK, or ATF2. Moreover, the p300 binding site and two CCAAT boxes in the RhoB promoter appear to be involved in ROS-mediated RhoB expression in the presence of KR28. Conclusion: The antitumor agent KR28 induces apoptosis of PC-3 cells by ROS-mediated RhoB expression via c-Abl upregulation and activation of p38 MAPK/ATF-2.-
dc.publisherSpringer-
dc.titleA novel antitumor piperazine alkyl compound causes apoptosis by inducing RhoB expression via ROS-mediated c-Abl/p38 MAPK signaling-
dc.title.alternativeA novel antitumor piperazine alkyl compound causes apoptosis by inducing RhoB expression via ROS-mediated c-Abl/p38 MAPK signaling-
dc.typeArticle-
dc.citation.titleCancer Chemotherapy and Pharmacology-
dc.citation.number0-
dc.citation.endPage1324-
dc.citation.startPage1315-
dc.citation.volume72-
dc.contributor.affiliatedAuthorKyung-Sook Chung-
dc.contributor.affiliatedAuthorBo Kyung Kim-
dc.contributor.affiliatedAuthorJiwon Ahn-
dc.contributor.affiliatedAuthorMi Sun Won-
dc.contributor.alternativeName정경숙-
dc.contributor.alternativeName한균희-
dc.contributor.alternativeName김보경-
dc.contributor.alternativeName김환묵-
dc.contributor.alternativeName양지선-
dc.contributor.alternativeName안지원-
dc.contributor.alternativeName이경-
dc.contributor.alternativeName송경빈-
dc.contributor.alternativeName원미선-
dc.identifier.bibliographicCitationCancer Chemotherapy and Pharmacology, vol. 72, pp. 1315-1324-
dc.identifier.doi10.1007/s00280-013-2310-y-
dc.subject.keywordc-Abl-
dc.subject.keywordp38 MAPK-
dc.subject.keywordProstate cancer-
dc.subject.keywordRhoB-
dc.subject.keywordROS-
dc.subject.localc-Abl-
dc.subject.localp38 MAP kinase-
dc.subject.localp38 mitogen-activated protein kinase (p38 MARK)-
dc.subject.localP38 MAPK-
dc.subject.localp38 mitogen-activated protein kinase-
dc.subject.localp38 MAPK-
dc.subject.localp38MAPK-
dc.subject.localprostate cancer-
dc.subject.localProstate cancer-
dc.subject.localRhoB-
dc.subject.localRhob-
dc.subject.localReactive oxidative species-
dc.subject.localReactive oxygen species(ROS)-
dc.subject.localReactive oxygen species-
dc.subject.localReactive Oxygen Species (ROS)-
dc.subject.localReactive Oxygen Species-
dc.subject.localROS-
dc.subject.localReactive oxygen species (ROS)-
dc.subject.localreactive oxygen species-
dc.subject.localreactive oxygen species (ROS)-
dc.description.journalClassY-
Appears in Collections:
Division of Research on National Challenges > 1. Journal Articles
Division of Biomedical Research > Personalized Genomic Medicine Research Center > 1. Journal Articles
Division of Research on National Challenges > Stem Cell Convergenece Research Center > 1. Journal Articles
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