Tumor-treating fields induce autophagy by blocking the Akt2/miR29b axis in glioblastoma cells
DC Field | Value | Language |
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dc.contributor.author | Kim, Eun Ho | - |
dc.contributor.author | Jo, Yunhui | - |
dc.contributor.author | Sai, Sei | - |
dc.contributor.author | Park, Mung-Jin | - |
dc.contributor.author | Kim, Jeong-Yub | - |
dc.contributor.author | Kim, Jin Su | - |
dc.contributor.author | Lee, Yeon-Joo | - |
dc.contributor.author | Cho, Jae-Min | - |
dc.contributor.author | Kwak, Seo-Young | - |
dc.contributor.author | Baek, Jeong-Hwa | - |
dc.contributor.author | Jeong, Youn Kyoung | - |
dc.contributor.author | Song, Jie-Young | - |
dc.contributor.author | Yoon, Myonggeun | - |
dc.contributor.author | Hwang, Sang-Gu | - |
dc.date.accessioned | 2021-09-01T05:49:51Z | - |
dc.date.available | 2021-09-01T05:49:51Z | - |
dc.date.created | 2021-06-19 | - |
dc.date.issued | 2019-09-26 | - |
dc.identifier.issn | 0950-9232 | - |
dc.identifier.uri | https://scholar.korea.ac.kr/handle/2021.sw.korea/62834 | - |
dc.description.abstract | Tumor-treating fields (TTFs) - a type of electromagnetic field-based therapy using low-intensity electrical fields - has recently been characterized as a potential anticancer therapy for glioblastoma multiforme (GBM). However, the molecular mechanisms involved remain poorly understood. Our results show that the activation of autophagy contributes to the TTF-induced anti-GBM activity in vitro or in vivo and GBM patient stem cells or primary in vivo culture systems. TTF-treatment upregulated several autophagy-related genes (similar to 2-fold) and induced cytomorphological changes. TTF-induced autophagy in GBM was associated with decreased Akt2 expression, not Akt1 or Akt3, via the mTOR/p70S6K pathway. An Affymetrix GeneChip miRNA 4.0 Array analysis revealed that TTFs altered the expression of many microRNAs (miRNAs). TTF-induced autophagy upregulated miR-29b, which subsequently suppressed the Akt signaling pathway. A luciferase reporter assay confirmed that TTFs induced miR-29b to target Akt2, negatively affecting Akt2 expression thereby triggering autophagy. TTF-induced autophagy suppressed tumor growth in GBM mouse models subjected to TTFs as determined by positron emission tomography and computed tomography (PET-CT). GBM patient stem cells and a primary in vivo culture system with high Akt2 levels also showed TTF-induced inhibition. Taken together, our results identified autophagy as a critical cell death pathway triggered by TTFs in GBM and indicate that TTF is a potential treatment option for GBM. | - |
dc.language | English | - |
dc.language.iso | en | - |
dc.publisher | NATURE PUBLISHING GROUP | - |
dc.subject | CANCER | - |
dc.subject | PROLIFERATION | - |
dc.subject | EXPRESSION | - |
dc.subject | SURVIVAL | - |
dc.subject | PATHWAY | - |
dc.title | Tumor-treating fields induce autophagy by blocking the Akt2/miR29b axis in glioblastoma cells | - |
dc.type | Article | - |
dc.contributor.affiliatedAuthor | Yoon, Myonggeun | - |
dc.identifier.doi | 10.1038/s41388-019-0882-7 | - |
dc.identifier.scopusid | 2-s2.0-85072686584 | - |
dc.identifier.wosid | 000487856000005 | - |
dc.identifier.bibliographicCitation | ONCOGENE, v.38, no.39, pp.6630 - 6646 | - |
dc.relation.isPartOf | ONCOGENE | - |
dc.citation.title | ONCOGENE | - |
dc.citation.volume | 38 | - |
dc.citation.number | 39 | - |
dc.citation.startPage | 6630 | - |
dc.citation.endPage | 6646 | - |
dc.type.rims | ART | - |
dc.type.docType | Article | - |
dc.description.journalClass | 1 | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.relation.journalResearchArea | Biochemistry & Molecular Biology | - |
dc.relation.journalResearchArea | Oncology | - |
dc.relation.journalResearchArea | Cell Biology | - |
dc.relation.journalResearchArea | Genetics & Heredity | - |
dc.relation.journalWebOfScienceCategory | Biochemistry & Molecular Biology | - |
dc.relation.journalWebOfScienceCategory | Oncology | - |
dc.relation.journalWebOfScienceCategory | Cell Biology | - |
dc.relation.journalWebOfScienceCategory | Genetics & Heredity | - |
dc.subject.keywordPlus | CANCER | - |
dc.subject.keywordPlus | PROLIFERATION | - |
dc.subject.keywordPlus | EXPRESSION | - |
dc.subject.keywordPlus | SURVIVAL | - |
dc.subject.keywordPlus | PATHWAY | - |
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