Wnt signaling pathway；ErbB signaling pathway； Calcium signaling pathway；HIF-1 signaling pathway；GnRH signaling pathway；Proteoglycans in cancer；Oocyte meiosis；Circadian entrainment；Long-term potentiation；Glioma；Neurotrophin signaling pathway；Cholinergic synapse；Amphetamine addiction；Gastric acid secretion；Dopaminergic synapse；Melanogenesis；Tuberculosis；Insulin secretion； Olfactory transduction

We also identified that CaMKIIδ was a direct target of miR-675 and partially mediated the effect of H19 on cardiomyocyte hypertrophy.

The H19 long noncoding RNA is a novel negative regulator of cardiomyocyte hypertrophy

Overexpression of H19 and miR-675 inhibited adipogenesis, while knockdown of their endogenous expression accelerated adipogenic differentiation. Mechanistically, we found that miR-675 targeted the 3' untranslated regions of the histone deacetylase (HDAC) 4-6 transcripts and resulted in deregulation of HDACs 4-6, essential molecules in adipogenesis.

Long Non-coding RNA H19 Inhibits Adipocyte Differentiation of Bone Marrow Mesenchymal Stem Cells through Epigenetic Modulation of Histone Deacetylases

Increasing the level of the RNA-binding protein HuR in cells overexpressing H19 prevented the stimulation of miR-675 processing from H19, promoted ZO-1 and E-cadherin expression, and restored the epithelial barrier function to a nearly normal level.

H19 Long Noncoding RNA Regulates Intestinal Epithelial Barrier Function via MicroRNA 675 by Interacting with RNA-Binding Protein HuR

MAPK signaling pathway；Cell cycle；Epstein-Barr virus infection；p53 signaling pathway；PI3K-Akt signaling pathway；Apoptosis；Thyroid cancer；Melanoma；Basal cell carcinoma；Measles；Chronic myeloid leukemia；Wnt signaling pathway；Neurotrophin signaling pathway；HTLV-I infection；Non-small cell lung cancer；Proteoglycans in cancer；Prostate cancer；Amyotrophic lateral sclerosis (ALS)；Transcriptional misregulation in cancer；Pathways in cancer；Pancreatic cancer；Huntington's disease；Hepatitis C；Colorectal cancer；Glioma；Bladder cancer；Endometrial cancer；Hepatitis B；Viral carcinogenesis；Small cell lung cancer；Herpes simplex infection

Ectopic expression of H19 significantly increased bladder cancer cell proliferation and miR-675 expression in vitro. Furthermore, overexpression of miR-675 promoted bladder cancer cell proliferation, while suppression of miR-675 induced G1 phase cell cycle arrest and promoted cell apoptosis. Western blotting analysis further identified that miR-675 inhibited p53 activation, decreased the ratio of Bax/Bcl-2 and cyclin D1 expression in bladder cancer cells； those effects may result in the abnormal proliferation of bladder cancer cells.

H19-derived miR-675 contributes to bladder cancer cell proliferation by regulating p53 activation

p53 signaling pathway；Inositol phosphate metabolism；Prostate cancer；Phosphatidylinositol signaling system；mTOR signaling pathway；PI3K-Akt signaling pathway；Focal adhesion；Tight junction；Hepatitis B；Pathways in cancer；Melanoma；Endometrial cancer；Glioma；Small cell lung cancer

LncRNA H19-derived microRNA (miR-675) are overexpressed in neointima of balloon-injured artery. We further validated that PTEN is the target gene of miR-675 as demonstrated by luciferase assay. Finally, the results of the rescue experiment indicated that LncRNA H19 promoted the proliferation of T/G HA-VSMC in a miR-675-dependent manner.

Long noncoding RNA H19-derived miR-675 aggravates restenosis by targeting PTEN

Pathways in cancer；Transcriptional misregulation in cancer；Chronic myeloid leukemia；Acute myeloid leukemia

To our knowledge, this is the time to demonstrate that RUNX1 serves as a link between H19/miR-675 axis and Akt/mTOR signaling and is a pivotal mediator in gastric cancer progression induced by H19/miR-675.

Long Noncoding RNA H19-Derived miR-675 Enhances Proliferation and Invasion via RUNX1 in Gastric Cancer Cells

In summary, melatonin antagonized premature senescence of CPCs via H19/miR-675/USP10 pathway, which provides new insights into pharmacological actions and potential applications of melatonin on the senescence of CPCs.

Long noncoding RNA H19 mediates melatonin inhibition of premature senescence of c-kit(+) cardiac progenitor cells by promoting miR-675

Calcium signaling pathway；Parkinson's disease；Huntington's disease；Influenza A；HTLV-I infection

In conclusion, our study demonstrates that H19/miR-675 axis is involved in the regulation of high glucose-induced apoptosis by targeting VDAC1, which may provide a novel therapeutic strategy for the treatment of DCM.

lncRNA H19/miR-675 axis regulates cardiomyocyte apoptosis by targeting VDAC1 in diabetic cardiomyopathy