Inhibition of NF-κB sensitizes human pancreatic carcinoma cells to apoptosis induced by etoposide (VP16) or doxorubicin View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2001-02

AUTHORS

Alexander Arlt, Jens Vorndamm, Maike Breitenbroich, Ulrich R Fölsch, Holger Kalthoff, Wolfgang E Schmidt, Heiner Schäfer

ABSTRACT

The transcription factor NF-kappaB has anti-apoptotic properties and may confer chemoresistance to cancer cells. Here, we describe human pancreatic carcinoma cell lines that differ in the responsiveness to the topoisomerase-2 inhibitors VP16 (20 microM) and doxorubicin (0.3 microM): Highly sensitive T3M4 [corrected] and PT45-P1 cells, and Capan-1 and A818-4 cells that were almost resistant to both anti cancer drugs. VP16, but not doxorubicin, transiently induced NF-kappaB activity in all cell lines, whereas basal NF-kappaB binding was nearly undetectable in T3M4 [corrected] and PT45-P1 cells, but rather high in Capan-1 and A818-4 cells, as demonstrated by gel-shift and luciferase assays. Treatment with various NF-kappaB inhibitors (Gliotoxin, MG132 and Sulfasalazine), or transfection with the IkappaBalpha super-repressor, strongly enhanced the apoptotic effects of VP16 or doxorubicin on resistant Capan-1 and 818-4 cells. Our results indicate that under certain conditions the resistance of pancreatic carcinoma cells to chemotherapy is due to their constitutive NF-kappaB activity rather than the transient induction of NF-kappaB by some anti-cancer drugs. Blockade of basal NF-kappaB activity by well established drugs efficiently reduces chemoresistance of pancreatic cancer cells and offers the potential for improved therapeutic strategies. More... »

PAGES

1204168

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/sj.onc.1204168

DOI

http://dx.doi.org/10.1038/sj.onc.1204168

DIMENSIONS

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PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/11314019


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