Retinoblastoma protein-interacting zinc finger 1, a tumor suppressor, augments lipopolysaccharide-induced proinflammatory cytokine production via enhancing nuclear factor-κB activation

Abu Shadat Mohammod Noman, Naoki Koide, Imtiaz Iftakhar-E-Khuda, Jargalsaikhan Dagvadorj, Gantsetseg Tumurkhuu, Yoshikazu Naiki, Takayuki Komatsu, Tomoaki Yoshida, Takashi Yokochi

Research output: Contribution to journalArticlepeer-review

6 Citations (Scopus)

Abstract

The involvement of retinoblastoma protein-interacting zinc finger 1 (RIZ1), a tumor suppressor, in lipopolysaccharide (LPS)-induced inflammatory responses was investigated by using RAW 264.7 macrophage-like cells. LPS significantly augmented the expression of RIZ1 and the augmentation was mediated by the activation of nuclear factor (NF)-κB and Akt. The silencing of RIZ1 with the siRNA led to the inactivation of NF-κB in response to LPS. Moreover, the RIZ1 silencing caused the down-regulation of p53 activation and a p53 pharmacological inhibitor attenuated the RIZ1 expression. LPS-induced tumor necrosis factor-α and interleukin-6 production was prevented by RIZ1 siRNA or a p53 pharmacological inhibitor. Therefore, RIZ1 was suggested to augment LPS-induced NF-κB activation in collaboration with p53 and enhance the production of proinflammatory cytokines in response to LPS.

Original languageEnglish
Pages (from-to)114-118
Number of pages5
JournalCellular Immunology
Volume264
Issue number2
DOIs
Publication statusPublished - 2010
Externally publishedYes

All Science Journal Classification (ASJC) codes

  • Immunology

Fingerprint

Dive into the research topics of 'Retinoblastoma protein-interacting zinc finger 1, a tumor suppressor, augments lipopolysaccharide-induced proinflammatory cytokine production via enhancing nuclear factor-κB activation'. Together they form a unique fingerprint.

Cite this