Repository logo
  • English
  • 中文
  • Log In
    New user? Click here to register.Have you forgotten your password?
Repository logo
    Communities & Collections
    Research Outputs
    Fundings & Projects
    People
    Organizations
    Statistics
  • English
  • 中文
  • Log In
    New user? Click here to register.Have you forgotten your password?
  1. Home
  2. Chung Shan Medical University
  3. Pure學術人才庫轉入
  4. GO-Y078 Triggers Program Cell Death in Human Cervical Cancer Cells Via MAPK Activation-Dependent Apoptotic Caspases Signaling
 
  • Details
Options

GO-Y078 Triggers Program Cell Death in Human Cervical Cancer Cells Via MAPK Activation-Dependent Apoptotic Caspases Signaling

Journal
Integrative Cancer Therapies
Date Issued
2026-01-01
Author(s)
YI-HSIEN HSIEH  
SHUN-FA YANG  
PEI-NI CHEN  
DOI
10.1177/15347354251411859
URI
https://www.scopus.com/pages/publications/105037562485
https://scholars.csmu.edu.tw/handle/123456789/30417
Abstract
Apoptosis is a regulated process of programed cell death that removes damaged ells. GO-Y078, a new curcumin analog, has been studied in the oncology field and shown to exert anti-proliferative and anti-angiogenic effects in multiple tumor types. However, its detailed signaling mechanisms and functional effects in human cervical cancer have not been clarified. Herein, GO-Y078 was employed to examine the anti-cancer mechanism in cervical cancer cells. GO-Y078 reduced the cell viability and elicited chromatin condensation and apoptotic cells of human cervical SiHa and HeLa cancer cells. Active PARP and active caspase-9, -8, and -3 were involved in GO-Y078-stimulated apoptosis. GO-Y078 also elevated phosphorylation of mitogen-activated protein kinase (MAPK) pathway. Co-treatment with GO-Y078 and either the ERK inhibitor U0126 or the p38 inhibitor SB203580 significantly reduced GO-Y078-induced activation of caspase-9, -8, and -3. In conclusion, GO-Y078 is a potential therapeutic candidate that induces apoptotic cell death in cervical cancer cells through phosphorylation-dependent activation of MAPK signaling followed by caspase activation.
Type
journal article
Make it your own

DSpace-CRIS can be extensively configured to meet your needs. Decide which information need to be collected and available with fine-grained security. Start updating the theme to match your Institution's web identity.

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

  • Cookie settings
  • Privacy policy
  • End User Agreement
  • Send Feedback