Dopaminergic synapse；MAPK signaling pathway；PI3K-Akt signaling pathway；Insulin secretion； Estrogen signaling pathway；Cocaine addiction；Epstein-Barr virus infection； Amphetamine addiction；Alcoholism； Hepatitis B；Influenza A； HTLV-I infection；Viral carcinogenesis

UCA1 directly interacted with miR-204 and decreased the binding of miR-204 to ATF2 3'UTR, which suppressed the degradation of ATF2 mRNA by miR-204.

Long non-coding RNA UCA1 promotes cell progression by acting as a competing endogenous RNA of ATF2 in prostate cancer

Dopaminergic synapse；MAPK signaling pathway；PI3K-Akt signaling pathway；Insulin secretion； Estrogen signaling pathway；Cocaine addiction；Epstein-Barr virus infection； Amphetamine addiction；Alcoholism； Hepatitis B；Influenza A； HTLV-I infection；Viral carcinogenesis

Silencing of hsa_circ_0001859 suppressed ATF2 expression and decreased inflammatory activity in SW982 cells. Hsa_circ_0001859 could compete with ATF2 for miR-204/211.

Hsa_circ_0001859 Regulates ATF2 Expression by Functioning as an MiR-204/211 Sponge in Human Rheumatoid Arthritis

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

By using online tools and a series of mechanistic analysis, we also demonstrated that miR-204-dependent CXCR4 regulation was required in MALAT1 modulating HCCA cell growth, migration and invasion. Taken together, our data indicated that MALAT1 might play an oncogenic role in HCCA through miR-204-dependent CXCR4 regulation, and could be regarded as a therapeutic target in HCCA.

Long Non-Coding RNA MALAT1 Interacted with miR-204 to Modulates Human Hilar Cholangiocarcinoma Proliferation, Migration and Invasion by Targeting CXCR4

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

Knockdown of MALAT1 inhibited the proliferation, migration, and invasion of human HCCA cell. In addition, chemokine receptor-4 (CXCR4) was involved in MALAT1 induced human HCCA growth, migration, and invasion. By using online tools and a series of mechanistic analysis, we also demonstrated that miR-204-dependent CXCR4 regulation was required in MALAT1 modulating HCCA cell growth, migration and invasion.

Long Non-Coding RNA MALAT1 Interacted with miR-204 to Modulates Human Hilar Cholangiocarcinoma Proliferation, Migration and Invasion by Targeting CXCR4

Amphetamine addiction

Mechanistically, ADNCR inhibited adipocyte differentiation by functioning as a competing endogenous RNA (ceRNA) for miR-204, thereby augmenting the expression of the miR-204 target gene, SIRT1, which is known to inhibit adipocyte differentiation and adipogenic gene expression by docking with NCoR and SMART to repress PPARγ activity

Long non-coding RNA ADNCR suppresses adipogenic differentiation by targeting miR-204

Hippo signaling pathway；Adherens junction

In particular, MALAT1 upregulated the expression of miR-204 target gene SLUG through competitively 'spongeing' miR-204.

LncRNA MALAT1 exerts oncogenic functions in lung adenocarcinoma by targeting miR-204

Pancreatic cancer；Cell cycle；Wnt signaling pathway；TGF-beta signaling pathway；Hippo signaling pathway；Adherens junction；Hepatitis B；HTLV-I infection；Pathways in cancer；Colorectal cancer；Chronic myeloid leukemia

In vitro experiments revealed that MALAT1 acted as a positive regulator of osteogenic differentiation by repressing miR-204 expression and activity and thereby promoting expression of osteoblast-specific markers, including alkaline phosphatase, mineralized bone matrix formation and osteocalcin. Mechanistically, we identified Smad4 as a direct target of miR-204. Importantly, MALAT1 could directly interact with miR-204 and overexpression of miR-204 efficiently reversed the upregulation of Smad4 induced by MALAT1. Thus, MALAT1 positively regulated the expression of Smad4 through sponging miR-204, and promoted osteogenic differentiation of VICs.

LncRNA MALAT1 sponges miR-204 to promote osteoblast differentiation of human aortic valve interstitial cells through up-regulating Smad4.

Cell cycle； Wnt signaling pathway；TGF-beta signaling pathway；Hippo signaling pathway；Adherens junction；Hepatitis B；HTLV-I infection；Pathways in cancer； Colorectal cancer；Pancreatic cancer；Chronic myeloid leukemia

Mechanistically, we identified Smad4 as a direct target of miR-204. Importantly, MALAT1 could directly interact with miR-204 and overexpression of miR-204 efficiently reversed the upregulation of Smad4 induced by MALAT1.

LncRNA MALAT1 sponges miR-204 to promote osteoblast differentiation of human aortic valve interstitial cells through up-regulating Smad4.

UCA1 directly interacted with miR-204 and decreased the binding of miR-204 to Sox4 3'UTR, which suppressed the degradation of Sox4 mRNA by miR-204.

lncRNA-UCA1 enhances cell proliferation through functioning as a ceRNA of Sox4 in esophageal cancer

Transcriptional misregulation in cancer

ZEB1 was identified as a downstream target of miR-204 and NEAT1 upregulated ZEB1 expression by negatively regulating miR-204 expression.

The long non-coding RNA NEAT1 regulates epithelial to mesenchymal transition and radioresistance in through miR-204/ZEB1 axis in nasopharyngeal carcinoma