YM155 sensitizes TRAIL-induced apoptosis through cathepsin S-dependent down-regulation of Mcl-1 and NF-&#x03BA;B-mediated down-regulation of c-FLIP expression in human renal carcinoma Caki cells

Seon Min Woo; Kyoung-jin Min; Bo Ram Seo; Taeg Kyu Kwon

doi:10.18632/oncotarget.11137

Oncotarget

Oncotarget (a primarily oncology-focused, peer-reviewed, open access journal) aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science.

Its scope is unique. The term "oncotarget" encompasses all molecules, pathways, cellular functions, cell types, and even tissues that can be viewed as targets relevant to cancer as well as other diseases. The term was introduced in the inaugural Editorial, Introducing Oncotarget.

As of January 1, 2022, Oncotarget has shifted to a continuous publishing model. Papers will now be published continuously within yearly volumes in their final and complete form and then quickly released to Pubmed.

Subscribe to receive alerts once a paper has been published by Oncotarget.

Learn about our FREE

Post-Publication Promotion Services

50% on all publication fees until the end of 2024.

Impact Journals, LLC is the publisher of Oncotarget: www.impactjournals.com.

Impact Journals is a member of the Wellcome Trust List of Compliant Publishers.

Impact Journals is a member of the Society for Scholarly Publishing.

On December 23, 2022, Oncotarget server experienced a DDoS attack. As a result, Oncotarget site was inaccessible for a few hours. Oncotarget team swiftly dealt with the situation and took it under control. This malicious action will be reported to the FBI.

Research Papers:

YM155 sensitizes TRAIL-induced apoptosis through cathepsin S-dependent down-regulation of Mcl-1 and NF-κB-mediated down-regulation of c-FLIP expression in human renal carcinoma Caki cells

Seon Min Woo, Kyoung-jin Min, Bo Ram Seo and Taeg Kyu Kwon _

PDF | HTML | Supplementary Files | How to cite

Oncotarget. 2016; 7:61520-61532. https://doi.org/10.18632/oncotarget.11137

Metrics: PDF 1828 views | HTML 2777 views | ?

Abstract

Seon Min Woo1,*, Kyoung-jin Min1,*, Bo Ram Seo1, Taeg Kyu Kwon1

1Department of Immunology, School of Medicine, Keimyung University, Dalseo-Gu, Daegu 704-701, South Korea

*These authors have contributed equally to this work

Correspondence to:

Taeg Kyu Kwon, email: [email protected]

Keywords: YM155, TRAIL, Mcl-1, c-FLIP, lysosome, NF-κB

Received: April 4, 2016 Accepted: July 27, 2016 Published: August 9, 2016

ABSTRACT

YM155, a small-molecule survivin inhibitor, has been reported for its anti-cancer activity in various cancer cells. In this study, we investigated the effect of YM155 to enhance TRAIL-mediated apoptosis in human renal carcinoma cells. We found that YM155 alone had no effect on apoptosis, however, combined treatment with YM155 and TRAIL markedly induced apoptosis in human renal carcinoma cells (Caki, ACHN, and A498), breast cancer cells (MDA-MB231), and glioma cells (U251MG), but not normal cells [mesangial cell (MC) and human skin fibroblast (HSF)]. YM155 induced down-regulation of Mcl-1 expression at the post-translational levels, and the overexpression of Mcl-1 markedly inhibited YM155 plus TRAIL-induced apoptosis. Furthermore, YM155 induced down-regulation of c-FLIP mRNA expression through inhibition of NF-κB transcriptional activity. Ectopic expression of c-FLIP markedly blocked YM155-induced TRAIL sensitization. Taken together, our results suggested that YM155 sensitizes TRAIL-mediated apoptosis via down-regulation of Mcl-1 and c-FLIP expression in renal carcinoma Caki cells.

All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 4.0 License.
PII: 11137

Publication Alerts

Post-Publication Promotion

Publication Discount

Research Papers:

YM155 sensitizes TRAIL-induced apoptosis through cathepsin S-dependent down-regulation of Mcl-1 and NF-κB-mediated down-regulation of c-FLIP expression in human renal carcinoma Caki cells

Abstract