NDLI: Sulforaphane potentiates growth-inhibiting and apoptosis-promoting activities of cisplatin following oxidative stress and mitochondrial dysfunction in malignant mesothelioma cells

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Sulforaphane potentiates growth-inhibiting and apoptosis-promoting activities of cisplatin following oxidative stress and mitochondrial dysfunction in malignant mesothelioma cells

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Molecular & Cellular Toxicology : Volume 12, Issue 2, June 2016

Molecular & Cellular Toxicology : Volume 12, Issue 1, March 2016

Molecular & Cellular Toxicology : Volume 11

Molecular & Cellular Toxicology : Volume 10

Molecular & Cellular Toxicology : Volume 9

Molecular & Cellular Toxicology : Volume 8

Molecular & Cellular Toxicology : Volume 7

Molecular & Cellular Toxicology : Volume 6

Sulforaphane potentiates growth-inhibiting and apoptosis-promoting activities of cisplatin following oxidative stress and mitochondrial dysfunction in malignant mesothelioma cells

Content Provider	Springer Nature Link
Author	Lee, Yoon Jin Lee, Sang Han
Copyright Year	2016
Abstract	Functional defects in apoptosis signaling have been considered the important mechanism of chemoresistance in malignant mesothelioma (MM). This study was designed to explore the growth-inhibiting and apoptosis-promoting effects of sulforaphane and cisplatin on the human MM cell lines, MSTO-211H and H-2452, and examine the underlying mechanisms. Compared to normal mesothelial Met-5A cells, sulforaphane and cisplatin exhibited synergistic anti-cancer efficacy towards MM cells. By inducing ROS accumulation and mitochondrial dysfunction, sulforaphane potentiated cisplatin-induced cytotoxic effects, as evidenced by the increased nuclear fragmentation and chromatin condensation with the enhanced cleavage of procaspase-3 and PARP, the increased percentage of Annexin V-PE (+) cells, and the appearance of a sub-G$_{0}$/G$_{1}$ peak in the flow cytometric analysis. The apoptosis-inducing effects of two compounds were associated with the increased Bax/Bcl-2 ratio due to a decrease in the anti-apoptotic Bcl-2 level. A G$_{2}$/M phase transition delay in the cell cycle following the combined treatment of sulforaphane and cisplatin was linked to the down-regulation of cyclin B1 and phospho-Cdc2 (Thr$^{161}$) levels. In addition, the inhibition of ROS with N-acetylcysteine attenuated the apoptosis induced by the combination treatment, and recovered the depletion of mitochondrial membrane potential, revealing the vital role of ROS in the synergism. By targeting redox homeostasis, such a pro-oxidant-based combinational approach will help to enhance the therapeutic efficacy and preferential cytotoxicity on MM cells that conventional therapy would be ineffective.
Starting Page	289
Ending Page	299
Page Count	11
File Format	PDF
ISSN	1738642X
Journal	Molecular & Cellular Toxicology
Volume Number	12
Issue Number	3
e-ISSN	20928467
Language	English
Publisher	The Korean Society of Toxicogenomics and Toxicoproteomics
Publisher Date	2016-10-07
Publisher Place	Incheon
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Sulforaphane Cisplatin Reactive oxygen species Mitochondrial membrane potential Apoptosis Cell Biology Pharmacology/Toxicology
Content Type	Text
Resource Type	Article
Subject	Health, Toxicology and Mutagenesis Public Health, Environmental and Occupational Health Toxicology Pathology and Forensic Medicine

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