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Updated: Oct 3, 2026

Generation of a RIP1 Knockout U937 Cell Line Using the CRISPR-Cas9 System
Published on: April 11, 2025
Cycloprodigiosin hydrocloride suppresses tumor necrosis factor (TNF) alpha-induced transcriptional activation by
1Department of Life Science, Faculty of Science, Himeji Institute of Technology, kamigori-chou, Akoh-gun, 678-1297, Hyogo, Japan.
Abstract:
Cycloprodigiosin hydrochloride (cPrG.HCl) obtained from a marine bacterium Pseudoalteromonas denitrificans induces apoptotic cell death in various cancerous cell lines. cPrG.HCl alone caused a little cytotoxicity in HeLa cells, but it enhanced the apoptotic process progressively when co-administered with tumor necrosis factor (TNF)alpha. Here we studied the effect of cPrG.HCl on TNFalpha-induced activation of the transcription factor nuclear factor kappaB (NF-kappaB). Luciferase gene reporter assays revealed that cPrG.HCl potently suppressed the TNFalpha- and the phorbol myristate acetate-induced activation of NF-kappaB. The suppression occurred in the presence of imidazole, indicating that it was not related to the intracellular acidification resulting from the intrinsic H(+)/Cl(-) symporter activity of cPrG.HCl. cPrG.HCl inhibited neither the TNFalpha-induced phosphorylation and degradation of inhibitor of nuclear factor-kappaB, nor the subsequent nuclear translocation and DNA binding of NF-kappaB. cPrG.HCl also suppressed NF-kappaB-enhanced gene expression induced by Rac1, Cdc42, MEKK1, inhibitor of nuclear factor-kappaalpha (IKKalpha), IKKbeta, and a subunit of NF-kappaB, p65. These results indicate that cPrG.HCl suppresses NF-kappaB-dependent gene expression through the inhibition of transcriptional activation.
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