Long-term potentiation；MAPK signaling pathway；Calcium signaling pathway；Type II diabetes mellitus；Arrhythmogenic right ventricular cardiomyopathy (ARVC)；Cardiac muscle contraction；Vascular smooth muscle contraction；GnRH signaling pathway；Hypertrophic cardiomyopathy (HCM)；Circadian entrainment；Retrograde endocannabinoid signaling； Dopaminergic synapse；Glutamatergic synapse；Alzheimer's disease；Cholinergic synapse；Serotonergic synapse；Insulin secretion；Dilated cardiomyopathy；Amphetamine addiction；GABAergic synapse

Besides, the expression of miRNA-328 was negatively correlated with TCONS_00075467. We further demonstrated that TCONS_00075467 could sponge miRNA-328 in vitro and in vivo to regulate the downstream protein coding gene CACNA1C. In addition, miRNA-328 could partly reverse the effects of TCONS_00075467 on electrical remodeling.

Altered long non-coding RNA expression profile in rabbit atria with atrial fibrillation: TCONS_00075467 modulates atrial electrical remodeling by sponging miR-328 to regulate CACNA1C.

Moreover, PVT1 might inhibit the expression of miR-152 and increased the expression of CD151 and FGF2 through regulating miR-152. PVT1 was positively associated with CD151 and FGF2 expression in GC tissues.

Long Noncoding RNA PVT1 Acts as a "Sponge" to Inhibit microRNA-152 in Gastric Cancer Cells

Moreover, PVT1 might inhibit the expression of miR-152 and increased the expression of CD151 and FGF2 through regulating miR-152.

Long Noncoding RNA PVT1 Acts as a "Sponge" to Inhibit microRNA-152 in Gastric Cancer Cells.

HIF-1 signaling pathway；NF-kappa B signaling pathway；Protein processing in endoplasmic reticulum；Pathways in cancer；Small cell lung cancer；Prostate cancer；PI3K-Akt signaling pathway；Apoptosis；Focal adhesion； Neurotrophin signaling pathway；Cholinergic synapse；Amyotrophic lateral sclerosis (ALS)；Colorectal cancer；Hepatitis B；Epstein-Barr virus infection； Toxoplasmosis；Tuberculosis

The results of qRT-PCR and western-blot proved that the expression of microRNA-144 was significantly boosted and the expression level of c-Met mRNA and protein was inhibited after lncRNA-TUG1 was silenced

Inhibition of long non-coding RNA TUG1 on gastric cancer cell transference and invasion through regulating and controlling the expression of miR-144/c-Met axis

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

lncARSR promoted sunitinib resistance via competitively binding miR-34/miR-449 to facilitate AXL and c-MET expression in RCC cells.

Exosome-Transmitted lncARSR Promotes Sunitinib Resistance in Renal Cancer by Acting as a Competing Endogenous RNA

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

lncARSR promoted sunitinib resistance via competitively binding miR-34/miR-449 to facilitate AXL and c-MET expression in RCC cells.

Exosome-Transmitted lncARSR Promotes Sunitinib Resistance in Renal Cancer by Acting as a Competing Endogenous RNA

Moreover, LINC00858 functioned as a competitive endogenous RNA (ceRNA), effectively becoming sponge for miR-422a and thereby modulating the expression of kallikrein-related peptidase 4 (KLK4).

Long intergenic non-protein coding RNA 00858 functions as a competing endogenous RNA for miR-422a to facilitate the cell growth in non-small cell lung cancer

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.

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.

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.

Pyrimidine metabolism；One carbon pool by folate；Metabolic pathways

LncRNA MALAT1 inhibition re-sensitized TMZ resistant cells through up-regulating miR-203 and down-regulating TS expression. On the other hand, MALAT1 overexpression promoted resistance by suppressing miR-203 and promoting TS expression.

MALAT1 is a prognostic factor in glioblastoma multiforme and induces chemoresistance to temozolomide through suppressing miR-203 and promoting thymidylate synthase expression