Downregulation of Bcl-2, FLIP or IAPs (XIAP and survivin) by siRNAs sensitizes resistant melanoma cells to Apo2L/TRAIL-induced apoptosis View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2004-08

AUTHORS

M Chawla-Sarkar, S I Bae, F J Reu, B S Jacobs, D J Lindner, E C Borden

ABSTRACT

Melanoma cells are relatively resistant to Apo2L/TRAIL (TNF-related apoptosis-inducing ligand). We postulated that resistance might result from higher expression of inhibitors of apoptosis including Bcl-2, FLIP (FLICE-like inhibitory protein) or IAPs such as XIAP (X-linked inhibitor of apoptosis) or survivin. Compared to scrambled or mismatch controls, targeting individual inhibitors with siRNA (si-Bcl-2, si-XIAP, si-FLIP or si-Surv), followed by Apo2L/TRAIL resulted in marked increase in apoptosis in melanoma cells. Compared to Bcl-2 or FLIP, siRNAs against XIAP and survivin were most potent in sensitizing melanoma cells. A similar substantial increase in apoptosis was seen in renal carcinoma cells (SKRC-45, Caki-2), following the inhibition of either XIAP or survivin by siRNAs. Apo2L/TRAIL treatment in IAP-targeted cells resulted in cleavage of Bid, activation of caspase-9 and cleavage of PARP (poly ADP-ribose polymerase). Thus, Apo2L/TRAIL resistance can be overcome by interfering with expression of inhibitors of apoptosis regulating both extrinsic (death receptor) or intrinsic (mitochondrial) pathways of apoptosis in melanoma cells. More... »

PAGES

4401416

Journal

TITLE

Cell Death & Differentiation

ISSUE

8

VOLUME

11

Author Affiliations

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/sj.cdd.4401416

DOI

http://dx.doi.org/10.1038/sj.cdd.4401416

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1038685270

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/15118763


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