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

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

Cytokine-cytokine receptor interaction；Endocytosis；PI3K-Akt signaling pathway；Axon guidance；Focal adhesion；Adherens junction；Bacterial invasion of epithelial cells；Proteoglycans in cancer；Renal cell carcinoma；Melanoma；Epithelial cell signaling in Helicobacter pylori infection；Malaria；Pathways in cancer；Transcriptional misregulation in cancer

We isolated cells from the primary mammary tumor, the circulation, and metastatic lesions in the lung in TA2 mice and found that the long noncoding RNA (lncRNA) H19 mediated EMT and MET by differentially acting as a sponge for the microRNAs miR-200b/c and let-7b.

The lncRNA H19 mediates breast cancer cell plasticity during EMT and MET plasticity by differentially sponging miR-200b/c and let-7b.