Dopaminergic synapse；PI3K-Akt signaling pathway；HTLV-I infection；Huntington's disease；Hepatitis B；Osteoclast differentiation；Antigen processing and presentation；Circadian rhythm；Alcoholism；Circadian entrainment；Cholinergic synapse；Prostate cancer；Viral carcinogenesis；Cocaine addiction；Tuberculosis；Insulin secretion；Estrogen signaling pathway；Melanogenesis；Amphetamine addiction；Vasopressin-regulated water reabsorption

Furthermore, we demonstrated HULC may act as an endogenous 'sponge', which down-regulates a series of microRNAs (miRNAs) activities, including miR-372. Inhibition of miR-372 leads to reducing translational repression of its target gene, PRKACB, which in turn induces phosphorylation of CREB.

CREB up-regulates long non-coding RNA, HULC expression through interaction with microRNA-372 in liver cancer

Cytokine-cytokine receptor interaction；Chemokine signaling pathway；Endocytosis；Axon guidance；Leukocyte transendothelial migration；Intestinal immune network for IgA production

H19 and HULC functioned as competing endogenous RNAs (ceRNAs) by sponging let-7a/let-7b and miR-372/miR-373, respectively, which activate pivotal inflammation cytokine IL-6 and chemokine receptor CXCR4.

LncRNAs H19 and HULC, activated by oxidative stress, promote cell migration and invasion in cholangiocarcinoma through a ceRNA manner

Cytokine-cytokine receptor interaction；Chemokine signaling pathway；Endocytosis；Axon guidance；Leukocyte transendothelial migration；Intestinal immune network for IgA production

H19 and HULC functioned as competing endogenous RNAs (ceRNAs) by sponging let-7a/let-7b and miR-372/miR-373, respectively, which activate pivotal inflammation cytokine IL-6 and chemokine receptor CXCR4.

LncRNAs H19 and HULC, activated by oxidative stress, promote cell migration and invasion in cholangiocarcinoma through a ceRNA manner

Cytokine-cytokine receptor interaction；Chemokine signaling pathway；Endocytosis；Axon guidance；Leukocyte transendothelial migration；Intestinal immune network for IgA production

H19 and HULC functioned as competing endogenous RNAs (ceRNAs) by sponging let-7a/let-7b and miR-372/miR-373, respectively, which activate pivotal inflammation cytokine IL-6 and chemokine receptor CXCR4.

LncRNAs H21 and HULC, activated by oxidative stress, promote cell migration and invasion in cholangiocarcinoma through a ceRNA manner

NOD-like receptor signaling pathway；Cytokine-cytokine receptor interaction；HIF-1 signaling pathway；PI3K-Akt signaling pathway；Toll-like receptor signaling pathway；Legionellosis；Hypertrophic cardiomyopathy (HCM)；African trypanosomiasis；Cytosolic DNA-sensing pathway；Jak-STAT signaling pathway；Hematopoietic cell lineage；Intestinal immune network for IgA production；Transcriptional misregulation in cancer；Influenza A； Herpes simplex infection；Pathways in cancer；Chagas disease (American trypanosomiasis)；Graft-versus-host disease；Malaria；Prion diseases；Pertussis；Rheumatoid arthritis；Measles；Salmonella infection；Amoebiasis；Hepatitis B；HTLV-I infection；Tuberculosis

H19 and HULC functioned as competing endogenous RNAs (ceRNAs) by sponging let-7a/let-7b and miR-372/miR-373, respectively, which activate pivotal inflammation cytokine IL-6 and chemokine receptor CXCR4.

LncRNAs H19 and HULC, activated by oxidative stress, promote cell migration and invasion in cholangiocarcinoma through a ceRNA manner

NOD-like receptor signaling pathway；Cytokine-cytokine receptor interaction；HIF-1 signaling pathway；PI3K-Akt signaling pathway；Toll-like receptor signaling pathway；Legionellosis；Hypertrophic cardiomyopathy (HCM)；African trypanosomiasis；Cytosolic DNA-sensing pathway；Jak-STAT signaling pathway；Hematopoietic cell lineage；Intestinal immune network for IgA production；Transcriptional misregulation in cancer；Influenza A； Herpes simplex infection；Pathways in cancer；Chagas disease (American trypanosomiasis)；Graft-versus-host disease；Malaria；Prion diseases；Pertussis；Rheumatoid arthritis；Measles；Salmonella infection；Amoebiasis；Hepatitis B；HTLV-I infection；Tuberculosis

H19 and HULC functioned as competing endogenous RNAs (ceRNAs) by sponging let-7a/let-7b and miR-372/miR-373, respectively, which activate pivotal inflammation cytokine IL-6 and chemokine receptor CXCR4.

LncRNAs H19 and HULC, activated by oxidative stress, promote cell migration and invasion in cholangiocarcinoma through a ceRNA manner