Table 1.

Functions of NF-κB associated lncRNAs.

NKILA

Binds with NF-κB p65-IκB complex in the cytoplasm, masks the phosphorylation motifs of IκB, inhibited IκB phosphorylation and NF-κB activation in breast cancer cells [16]. Modulated by NF-κB inducers in breast cancer cells [16]. Reduced the proliferation, migration and invasion, and induced apoptosis in melanoma cells [18]. Inversely correlated with lymph node metastasis and advanced TNM stage in NSCLC [19]; Reduced the migration and invasion of NSCLC cells [19]. Inversely associated with the tumor metastasis and poor prognosis of TSCC patients; reduced the IκBα phosphorylation, NF-κB activation, EMT, and migration and invasion of TSCC cells [20]. Enhanced the efficacy of baicalein in hepatocellular carcinoma cells [17].

Carlr

Suppressed mitochondrial fission and apoptosis by targeting miRNA-539 and PHB2 in cardiomyocytes [28]. Knockdown of Carlr impaired the expression of NF-κB related genes in mouse and human macrophages [29].

HOTAIR

HOTAIR expression is modulated by TNF-α [31] and NF-κB [32] in cancer cells. Enhanced TNF-α levels and p65 phosphorylation in septic mice model and in cardiomyocytes [34]. Induced the DNA damage response and reduced genomic integrity in ovarian cancer cells [32].

MALAT1

Regulated the production of cytokines in macrophages under inflammatory conditions [48]. Directly binds with p65 and p50, suppresses the NF-κB DNA binding, reduces TNF-α and IL-6 expression [48]. Suppressed the hypoxia-induced inflammatory response in the mice model of renal ischemia-reperfusion injury [50]. Up-regulated IL-6 and TNF-α in human umbilical vein endothelial cells in response to glucose [51]. Required for EMT mediated cell migration and invasion in OSCC cell lines [52].

ANRIL

Modulated the expression of NF-κB dependent inflammatory molecules such as IL-8 and IL-6 [57]. Induced VEGF expression and angiogenesis through NF-κB activation in the rat model of diabetes mellitus and cerebral infarction [59].

Lethe

Physically associate with p65, blocks DNA binding and reduces the production of inflammatory molecules; expression reduced in aged spleen [60]. Regulated ROS production in macrophages through modulation of NOX-2 and NF-κB [63].

MIR31HG

Expression promoted by the binding of p65 to the MIR31HG promoter; induces IκBα phosphorylation by direct interaction leading to NF-κB activation [66].

PACER

Modulated COX2 expression by occluding the binding of inhibitory p50/p50 homodimers and facilitating the active p65/p50 heterodimer formation at the COX2 promoter [67]. Regulated by COX2 [67].

lincRNA-Cox2

Highly induced upon LPS stimulation and during the innate immune response [71,131]. Required for the NF-κB-regulated late-primary inflammatory response genes transcription following LPS stimulation [72].

lincRNA-p21

Suppressed the NF-κB activity by inhibiting p65 mRNA translation [79]. Required for anti-inflammatory activities of MTX in RA patients [79].

C2dat1

Promoted the viability, migration, and invasion via interaction with Sirt1 and miR-34–5p in osteosarcoma cells [80]. Up-regulated CAMK2D expression and promoted neural survival in response to OGD/R [81].

Arid2-IR

Enhanced the NF-κB activity and the expression of pro-inflammatory cytokines induced by IL-1β [82].

Gm4419

Upregulated by OGD/R, induced IκBα phosphorylation by direct interaction leading to NF-κB activation; enhanced the IL-6, IL-1β and TNF-α transcription in microglial cells [84].

Mirt1

Induced NF-κB activation and inflammatory response in cardiomyocytes [87]. Deteriorated cardiac function, induced apoptosis and inflammatory cell infiltration in mice model of myocardial infarction [86].