MYD88 signals induce tumour-initiating cell generation through the NF-κB-HIF-1α activation cascade.

ABSTRACT: Tumour-promoting inflammation is a hallmark of cancer, and chronic inflammatory disease increases the risk of cancer. In this context, MYD88, a downstream signalling molecule of Toll-like receptors that initiates inflammatory signalling cascades, has a critical role in tumour development in mice and its gene mutation was found in human cancers. In inflammation-induced colon cancer, tumour suppressor p53 mutations have also been detected with high frequency as early events. However, the molecular mechanism of MYD88-induced cancer development is poorly understood. Here, we demonstrated that MYD88 induced the protein accumulation of the transcription factor HIF-1α through NF-κB in p53-deficient cells. HIF-1α accumulation was not caused by enhanced protein stability but by NF-κB-mediated trans

SUBMITTER: Tanimura A 

PROVIDER: S-EPMC7890054 | biostudies-literature | 2021 Feb

REPOSITORIES: biostudies-literature