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Cited 8 times in

The bifunctional autophagic flux by 2-deoxyglucose to control survival or growth of prostate cancer cells

DC FieldValueLanguage
dc.contributor.author김승원-
dc.contributor.author윤미진-
dc.contributor.author전정용-
dc.contributor.author박기청-
dc.date.accessioned2016-02-04T11:55:18Z-
dc.date.available2016-02-04T11:55:18Z-
dc.date.issued2015-
dc.identifier.issn1471-2407-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/141494-
dc.description.abstractBACKGROUND: Recent reports using metabolism regulating drugs showed that nutrient deprivation was an efficient tool to suppress cancer progression. In addition, autophagy control is emerging to prevent cancer cell survival. Autophagy breaks down the unnecessary cytoplasmic components into anabolic units and energy sources, which are the most important sources for making the ATP that maintains homeostasis in cancer cell growth and survival. Therefore, the glucose analog 2-deoxyglucose (2DG) has been used as an anticancer reagent due to its inhibition of glycolysis. METHODS: Prostate cancer cells (PC3) were treated with 2DG for 6 h or 48 h to analyze the changing of cell cycle and autophagic flux. Rapamycin and LC3B overexpressing vectors were administered to PC3 cells for autophagy induction and chloroquine and shBeclin1 plasmid were used to inhibit autophagy in PC3 cells to analyze PC3 cells growth and survival. The samples for western blotting were prepared in each culture condition to confirm the expression level of autophagy related and regulating proteins. RESULTS: We demonstrated that 2DG inhibits PC3 cells growth and had discriminating effects on autophagy regulation based on the different time period of 2DG treatment to control cell survival. Short-term treatment of 2DG induced autophagic flux, which increased microtubule associated protein 1 light chain 3B (LC3B) conversion rates and reduced p62 levels. However, 2DG induced autophagic flux is remarkably reduced over an extended time period of 2DG treatment for 48 h despite autophagy inducing internal signaling being maintained. The relationship between cell growth and autophagy was proved. Increased autophagic flux by rapamycin or LC3B overexpression powerfully reduced cell growth, while autophagy inhibition with shBeclin1 plasmid or chloroquine had no significant effect on regulating cell growth. CONCLUSION: Given these results, maintaining increased autophagic flux was more effective at inhibiting cancer cell progression than inhibition of autophagic flux, which is necessary for the survival of PC3 cells. Autophagic flux should be tightly regulated to maintain metabolic homeostasis for cancer cell growth and survival in PC3 cells and is a suitable target for cancer therapy.-
dc.description.statementOfResponsibilityopen-
dc.formatapplication/pdf-
dc.relation.isPartOfBMC Cancer-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.subject.MESHAntimetabolites/therapeutic use*-
dc.subject.MESHAutophagy/drug effects*-
dc.subject.MESHBlotting, Western-
dc.subject.MESHCell Cycle/drug effects-
dc.subject.MESHCell Line, Tumor-
dc.subject.MESHDeoxyglucose/therapeutic use*-
dc.subject.MESHDrug Evaluation, Preclinical-
dc.subject.MESHHumans-
dc.subject.MESHMale-
dc.subject.MESHMicroscopy, Confocal-
dc.subject.MESHMicrotubule-Associated Proteins/metabolism-
dc.subject.MESHProstatic Neoplasms/metabolism-
dc.subject.MESHProstatic Neoplasms/pathology*-
dc.titleThe bifunctional autophagic flux by 2-deoxyglucose to control survival or growth of prostate cancer cells-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentYonsei Biomedical Research Center (연세의생명연구원)-
dc.contributor.googleauthorJeong Yong Jeon-
dc.contributor.googleauthorSeung Won Kim-
dc.contributor.googleauthorKi Cheong Park-
dc.contributor.googleauthorMijin Yun-
dc.identifier.doi10.1186/s12885-015-1640-z-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.contributor.localIdA02550-
dc.contributor.localIdA03545-
dc.contributor.localIdA00656-
dc.relation.journalcodeJ00351-
dc.identifier.pmid26345371-
dc.subject.keywordRapamycin-
dc.subject.keywordEndoplasmic Reticulum Stress-
dc.subject.keywordLNCaP Cell-
dc.subject.keywordAutophagic Cell Death-
dc.subject.keywordAutophagy Inhibition-
dc.contributor.alternativeNameKim, Seung Won-
dc.contributor.alternativeNameYun, Mi Jin-
dc.contributor.alternativeNameJeon, Jeong Yong-
dc.contributor.affiliatedAuthorYun, Mi Jin-
dc.contributor.affiliatedAuthorJeon, Jeong Yong-
dc.contributor.affiliatedAuthorKim, Seung Won-
dc.rights.accessRightsfree-
dc.citation.volume15-
dc.citation.startPage623-
dc.identifier.bibliographicCitationBMC Cancer, Vol.15 : 623, 2015-
Appears in Collections:
1. College of Medicine (의과대학) > Yonsei Biomedical Research Center (연세의생명연구원) > 1. Journal Papers
1. College of Medicine (의과대학) > BioMedical Science Institute (의생명과학부) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Nuclear Medicine (핵의학교실) > 1. Journal Papers

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