Table 1.

Cytoplasmic lncRNAs in cancer signaling pathways

Gene	Main distribution	Related signaling pathway	Mechanism	Reference
LINK-A	Triple-negative breast tumor	HIF-1α	Mediates HB-EGF triggered, EGFR:GPNMB heterodimer-dependent HIF-1α phosphorylation, leading to HIF-1α stabilization and activation of HIF-1α transcriptional programs	Lin et al., 2016
		PI3K/AKT	Contributes to the AKT-PIP3 interaction and enhances EGF-induced AKT kinase activity	Lin et al., 2017
MAYA	Majority of human solid tumors	Hippo-YAP	HER3-LLGL2-MAYA-NSUN6 complex methylates MST1 to activate YAP and target genes	Li et al., 2017
Lnc-DC	Dendritic cells	STAT3	Promotes STAT3 phosphorylation	Zhong et al., 1999
NKILA	Normal breast epithelia or non-invasive breast tumors	NF-κB	Inhibits IKK-induced IκB phosphorylation to restrain NF-κB activity	Liu et al., 2015
ACOD1	Most of the cells and organs	GOT2 metabolic pathway	Binds the metabolic enzyme GOT2 and enhances its catalytic activity	Wang et al., 2017
Lnc-Lsm3b	Immune cells and organs	IFN I	Binds to RIG-I and inhibits its activation to terminate type I IFN production	Jiang et al., 2018

HIF-1α: hypoxia-inducible factor 1α; HB-EGF: heparin-binding epidermal growth factor; EGFR: EGF receptor; GPNMB: glycoprotein nonmetastatic melanoma protein B; PI3K: phosphoinositide 3-kinase; AKT: serine-threonine-protein kinase; STAT3: signal transducers and activators of transcription 3; NF-κB: nuclear factor-κB; IκB: inhibitor of NF-κB; IKK: IκB kinase; GOT2: glutamate-oxaloacetate transaminase 2; IFN: interferon; RIG-I: retinoic acid-inducible gene I