Fig. 2

Schematic illustration of JAK/STAT and IKK/NF-κB pathway linking inflammation and ncRNA transcription in TME. a Various inflammation-associated cytokines (IL-6/IL-8/IL-1β/TNF-α/IFNs) and chemokines bind directly to their receptors on cancer cell membrane and activate JAK tyrosine kinase. Activated JAK tyrosine kinase phosphorylates STAT. Phosphorylated STAT dimerizes and translocates into the nucleus, where it binds to the gene promoter regions and transcribes numerous ncRNAs. b In response to pro-inflammatory cytokines like TNF-α, IL-1β, IFNs, or chemokines, the formation of IKK protein complex, which consists of IKK-α, β, γ subunits, is activated. The IKK complex then phosphorylates the IκB subunit of NF-κB/IκB complex, thereby resulting in proteasomal degradation of IκB and the nuclear translocation of NF-κB dimers (p50/p65). The NF-κB (p50/p65) complex mediates the transcription of various noncoding genes through binding to their promoter regions