Repository logo
  • English
  • 中文
Log In
Have you forgotten your password?
  1. Home
  2. College of Medicine / 醫學院
  3. Toxicology / 毒理學研究所
  4. Improved effects of honokiol on temozolomide-induced autophagy and apoptosis of drug-sensitive and -tolerant glioma cells
 
  • Details

Improved effects of honokiol on temozolomide-induced autophagy and apoptosis of drug-sensitive and -tolerant glioma cells

Journal
BMC Cancer
Journal Volume
18
Journal Issue
1
Date Issued
2018
Author(s)
Chio C.-C.
Chen K.-Y.
Chang C.-K.
Chuang J.-Y.
Liu C.-C.
SHING-HWA LIU  
Chen R.-M.
DOI
10.1186/s12885-018-4267-z
URI
https://www.scopus.com/inward/record.uri?eid=2-s2.0-85044869266&doi=10.1186%2fs12885-018-4267-z&partnerID=40&md5=78ba2284bb0e3e4e69cf92954615cff8
https://scholars.lib.ntu.edu.tw/handle/123456789/431149
Abstract
Background: Temozolomide (TMZ)-induced side effects and drug tolerance to human gliomas are still challenging issues now. Our previous studies showed that honokiol, a major bioactive constituent of Magnolia officinalis (Houpo), is safe for normal brain cells and can kill human glioma cells. This study was further aimed to evaluate the improved effects of honokiol and TMZ on drug-sensitive and -resistant glioma cells and the possible mechanisms. Methods: TMZ-sensitive human U87-MG and murine GL261 glioma cells and TMZ-resistant human U87-MR-R9 glioma cells were exposed to honokiol and TMZ, and cell viability and LC50 of honokiol were assayed. To determine the death mechanisms, caspase-3 activity, DNA fragmentation, apoptotic cells, necrotic cells, cell cycle, and autophagic cells. The glioma cells were pretreated with 3-methyladenine (3-MA) and chloroquine (CLQ), two inhibitors of autophagy, and then exposed to honokiol or TMZ. Results: Exposure of human U87-MG glioma cells to honokiol caused cell death and significantly enhanced TMZ-induced insults. As to the mechanism, combined treatment of human U87-MG cells with honokiol and TMZ induced greater caspase-3 activation, DNA fragmentation, cell apoptosis, and cell-cycle arrest at the G1 phase but did not affect cell necrosis. The improved effects of honokiol on TMZ-induced cell insults were further verified in mouse GL261 glioma cells. Moreover, exposure of drug-tolerant human U87-MG-R9 cells to honokiol induced autophagy and consequent apoptosis. Pretreatments with 3-MA and CLQ caused significant attenuations in honokiol- and TMZ-induced cell autophagy and apoptosis in human TMZ-sensitive and -tolerant glioma cells. Conclusions: Taken together, this study demonstrated the improved effects of honokiol with TMZ on autophagy and subsequent apoptosis of drug-sensitive and -tolerant glioma cells. Thus, honokiol has the potential to be a drug candidate for treating human gliomas. ? 2018 The Author(s).
Subjects
Autophagy and apoptosis; Drug tolerance; Glioma cells; Honokiol; Temozolomide
SDGs

[SDGs]SDG3

Other Subjects
3 methyladenine; caspase 3; chloroquine; honokiol; temozolomide; antineoplastic agent; biphenyl derivative; caspase 3; honokiol; lignan; temozolomide; animal cell; antineoplastic activity; apoptosis; Article; autophagy; cancer combination chemotherapy; cancer resistance; cell cycle; cell viability; chemosensitivity; controlled study; DNA fragmentation; drug mechanism; drug potentiation; drug tolerance; enzyme activity; glioma cell; human; human cell; LC50; mouse; nonhuman; apoptosis; autophagy; cell cycle checkpoint; cell survival; drug effect; drug potentiation; drug resistance; glioma; metabolism; tumor cell line; Antineoplastic Agents, Phytogenic; Apoptosis; Autophagy; Biphenyl Compounds; Caspase 3; Cell Cycle Checkpoints; Cell Line, Tumor; Cell Survival; Drug Resistance, Neoplasm; Drug Synergism; Glioma; Humans; Lignans; Temozolomide
Publisher
BioMed Central Ltd.
Type
journal article

臺大位居世界頂尖大學之列,為永久珍藏及向國際展現本校豐碩的研究成果及學術能量,圖書館整合機構典藏(NTUR)與學術庫(AH)不同功能平台,成為臺大學術典藏NTU scholars。期能整合研究能量、促進交流合作、保存學術產出、推廣研究成果。

To permanently archive and promote researcher profiles and scholarly works, Library integrates the services of “NTU Repository” with “Academic Hub” to form NTU Scholars.

總館學科館員 (Main Library)
醫學圖書館學科館員 (Medical Library)
社會科學院辜振甫紀念圖書館學科館員 (Social Sciences Library)

開放取用是從使用者角度提升資訊取用性的社會運動,應用在學術研究上是透過將研究著作公開供使用者自由取閱,以促進學術傳播及因應期刊訂購費用逐年攀升。同時可加速研究發展、提升研究影響力,NTU Scholars即為本校的開放取用典藏(OA Archive)平台。(點選深入了解OA)

  • 請確認所上傳的全文是原創的內容,若該文件包含部分內容的版權非匯入者所有,或由第三方贊助與合作完成,請確認該版權所有者及第三方同意提供此授權。
    Please represent that the submission is your original work, and that you have the right to grant the rights to upload.
  • 若欲上傳已出版的全文電子檔,可使用Open policy finder網站查詢,以確認出版單位之版權政策。
    Please use Open policy finder to find a summary of permissions that are normally given as part of each publisher's copyright transfer agreement.
  • 網站簡介 (Quickstart Guide)
  • 使用手冊 (Instruction Manual)
  • 線上預約服務 (Booking Service)
  • 方案一:臺灣大學計算機中心帳號登入
    (With C&INC Email Account)
  • 方案二:ORCID帳號登入 (With ORCID)
  • 方案一:定期更新ORCID者,以ID匯入 (Search for identifier (ORCID))
  • 方案二:自行建檔 (Default mode Submission)
  • 方案三:學科館員協助匯入 (Email worklist to subject librarians)

Built with DSpace-CRIS software - Extension maintained and optimized by 4Science