Role of Death Receptors-associated Lipid Rafts in Oxaliplatin-induced Death Mode Regulation of HepG2 Cells.


Journal

Anticancer research
ISSN: 1791-7530
Titre abrégé: Anticancer Res
Pays: Greece
ID NLM: 8102988

Informations de publication

Date de publication:
May 2020
Historique:
received: 03 03 2020
revised: 13 03 2020
accepted: 16 03 2020
entrez: 6 5 2020
pubmed: 6 5 2020
medline: 19 5 2020
Statut: ppublish

Résumé

We previously showed that oxaliplatin induces necrotic-like cell death in hepatocarcinomas, and combination with ursodexoycholic acid (UDCA) significantly shifts the necrotic-like death to apoptosis. Since cell death mode is crucial on inflammatory responses and chemotherapeutic efficacy, the mechanism underlying determination of cell death mode by UDCA was investigated in this study. Apoptosis or necrosis was determined by apoptotic body formation, caspase-8 activity, LDH release and PI inclusion. The involvement of lipid rafts and death receptors was examined by rafts fractionation, confocal microscopy and gene silencing assays. UDCA combination enhanced recruitment of death receptors and adaptors into cholesterol-enriched lipid rafts, and induced a stronger raft clustering. Lipid raft disruption decreased the UDCA/oxaliplatin-mediated apoptosis and increased necrotic-like death. UDCA promotes lipid raft localization of multiple death receptors, thereby contributing to a shift of cell death mode from oxaliplatin-induced necrotic death to apoptosis in HepG2 cells.

Sections du résumé

BACKGROUND/AIM OBJECTIVE
We previously showed that oxaliplatin induces necrotic-like cell death in hepatocarcinomas, and combination with ursodexoycholic acid (UDCA) significantly shifts the necrotic-like death to apoptosis. Since cell death mode is crucial on inflammatory responses and chemotherapeutic efficacy, the mechanism underlying determination of cell death mode by UDCA was investigated in this study.
MATERIALS AND METHODS METHODS
Apoptosis or necrosis was determined by apoptotic body formation, caspase-8 activity, LDH release and PI inclusion. The involvement of lipid rafts and death receptors was examined by rafts fractionation, confocal microscopy and gene silencing assays.
RESULTS RESULTS
UDCA combination enhanced recruitment of death receptors and adaptors into cholesterol-enriched lipid rafts, and induced a stronger raft clustering. Lipid raft disruption decreased the UDCA/oxaliplatin-mediated apoptosis and increased necrotic-like death.
CONCLUSION CONCLUSIONS
UDCA promotes lipid raft localization of multiple death receptors, thereby contributing to a shift of cell death mode from oxaliplatin-induced necrotic death to apoptosis in HepG2 cells.

Identifiants

pubmed: 32366402
pii: 40/5/2573
doi: 10.21873/anticanres.14228
doi:

Substances chimiques

Biomarkers 0
RNA, Small Interfering 0
Receptors, Death Domain 0
Oxaliplatin 04ZR38536J

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

2573-2582

Informations de copyright

Copyright© 2020, International Institute of Anticancer Research (Dr. George J. Delinasios), All rights reserved.

Auteurs

Sung-Chul Lim (SC)

Department of Pathology, College of Medicine, Chosun University, Gwangju, Republic of Korea.
Research Center for Resistant Cells, Chosun University, Gwangju, Republic of Korea.

Keshab Raj Parajuli (KR)

Research Center for Resistant Cells, Chosun University, Gwangju, Republic of Korea.

Song Iy Han (SI)

Research Center for Resistant Cells, Chosun University, Gwangju, Republic of Korea sihan@chosun.ac.kr.
Division of Premedical Science, College of Medicine, Chosun University, Gwangju, Republic of Korea.

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Classifications MeSH