Nuclear factor-κB (NF-κB) signaling plays a pivotal role in GBM pathogenesis by promoting proliferation, invasion, inflammation, immune evasion, and treatment resistance.
First-pass extracted concept
NF-κB signaling in glioblastoma
Candidate: concept label1 source documents7 linked claims
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Aliases
NF-κB signaling, Nuclear factor-κB signaling in GBM
Evidence Snippets
Supporting Sources
Linked Claims
ncRNA-mediated epigenetic switches linked to NF-κB shape glioblastoma cell plasticity and subtype specification.
Quoted textsource-backed
novel ncRNA-mediated epigenetic switches that shape GBM cell plasticity and subtype specification
NF-κB signaling contributes to maintaining tumor stemness, metabolic adaptation, and angiogenesis in glioblastoma.
Quoted textsource-backed
roles in maintaining tumor stemness, metabolic adaptation, and angiogenesis
NF-κB signaling promotes proliferation, invasion, inflammation, immune evasion, and treatment resistance in glioblastoma.
Quoted textsource-backed
promoting proliferation, invasion, inflammation, immune evasion, and treatment resistance
NF-κB modulates the glioblastoma tumor microenvironment by orchestrating pro-tumorigenic cytokine production, immune cell reprogramming, and stromal remodeling.
Quoted textsource-backed
it orchestrates pro-tumorigenic cytokine production, immune cell reprogramming, and stromal remodeling
NF-κB signaling plays a pivotal role in glioblastoma pathogenesis.
Quoted textsource-backed
Nuclear factor-κB (NF-κB) signaling plays a pivotal role in GBM pathogenesis
NF-κB and non-coding RNAs, particularly microRNAs, have reciprocal regulatory dynamics in glioblastoma.
Quoted textsource-backed
the reciprocal regulatory dynamics between NF-κB and non-coding RNAs (ncRNAs), particularly microRNAs
NF-κB signaling in glioblastoma is discussed as interacting with STAT3, FOSL1, and TRPM7.
Quoted textsource-backed
interactions with key oncogenic factors (including STAT3, FOSL1, and TRPM7)