Dopaminergic synapse；ErbB signaling pathway；MAPK signaling pathway；Prostate cancer；Pathways in cancer；Melanoma；Pancreatic cancer；Chemokine signaling pathway；Fc epsilon RI signaling pathway；HIF-1 signaling pathway；Progesterone-mediated oocyte maturation；Colorectal cancer；HTLV-I infection；mTOR signaling pathway；Toll-like receptor signaling pathway；Toxoplasmosis；Epstein-Barr virus infection；Proteoglycans in cancer；Influenza A；Cholinergic synapse；Fc gamma R-mediated phagocytosis；Neurotrophin signaling pathway；Jak-STAT signaling pathway；T cell receptor signaling pathway；Acute myeloid leukemia；Glioma；Small cell lung cancer；Non-small cell lung cancer；PI3K-Akt signaling pathway； Apoptosis；VEGF signaling pathway；Hepatitis C；Carbohydrate digestion and absorption；Chagas disease (American trypanosomiasis)；Measles；Adipocytokine signaling pathway；Tuberculosis； Osteoclast differentiation；B cell receptor signaling pathway；Hepatitis B；Focal adhesion；Estrogen signaling pathway；Insulin signaling pathway；Tight junction；Endometrial cancer；Chronic myeloid leukemia；Renal cell carcinoma

In addition, overexpression of H19 in GBC-SD cells downregulated miR-194-5p and markedly increased AKT2 expression, and miR-194-5p mimic reversed these effects.

Long noncoding RNA H19 contributes to gallbladder cancer cell proliferation by modulated miR-194-5p targeting AKT2

Vasopressin-regulated water reabsorption

Here, we show that the human long noncoding RNA (lncRNA) H19 may function as a competing endogenous RNA (ceRNA) to regulate the expression of AQP3 through competition for miR-874, thus playing a significant role in maintaining intestinal barrier function.

LncRNA H19 functions as a competing endogenous RNA to regulate AQP3 expression by sponging miR-874 in the intestinal barrier

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

Calcium signaling pathway； Neuroactive ligand-receptor interaction；Gastric acid secretion

H19 upregulated the miRNA-148b target gene chole- cystokinin-2 receptor (CCK2R) by competitively `sponging' miRNA-148b and then promoted the proliferation and invasiveness of CRC cells.

Long non-coding RNA H19 promotes colorectal cancer metastasis via negative modulation of miR-148b

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 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

Cysteine and methionine metabolism；Metabolic pathways

We identified microRNA miR-148a-3p as an inhibitory target for H19. Overexpression of miR-148a-3p reduced LSCC migration, invasion and proliferation cell, while inhibition of miR-148a-3p did the opposite. The inhibition of LSCC progression induced by H19 knockdown required the activity of miR-148a-3p. We also identified DNA methyltransferase enzyme DNMT1 as a target of miR-148a-3p

Regulation of laryngeal squamous cell cancer progression by the lncRNA H19/miR-148a-3p/DNMT1 axis

Cysteine and methionine metabolism；Metabolic pathways

H19 act as an endogenous sponge by directly binding to miR-152. miR-152 directly targeted DNMT1 and was regulated by H19. Besides, H19 overexpression dramatically relieved the inhibition of miR-152 on DNMT1 expression. miR-152 inhibition and DNMT1 overexpression obviously reversed the inhibitory effects of H19 downregulation on cell proliferation and invasion.

Long non-coding RNA H19 promotes the proliferation and invasion of breast cancer through upregulating DNMT1 expression by sponging miR-152.

Glioma；Cell cycle；Hepatitis B；HTLV-I infection；Pathways in cancer；Pancreatic cancer；Prostate cancer；Melanoma；Bladder cancer；Non-small cell lung cancer； Chronic myeloid leukemia；Small cell lung cancer

We found that lncRNA H19 was increased in melanoma tissue, and lncRNA H19 was correlated with poor prognosis of melanoma patients. miR-106a-5p acts as a tumour suppressor in melanoma by targeting E2F3

Long non-coding RNA H19 promotes glucose metabolism and cell growth in malignant melanoma via miR-106a-5p/E2F3 axis

Rather than direct interaction, H19 regulated EZH2 expression by suppressing the activity of miR-630, which is a repressor of EZH2 and interacts with H19 in a sequence-specific manner.

Long noncoding RNA H19 regulates EZH2 expression by interacting with miR-630 and promotes cell invasion in nasopharyngeal carcinoma

QRT-PCR and Western-blotting assays demonstrated that H19 silencing down-regulated, whereas over-expression enhanced the expression of miR-342-3p targeting FOXM1 through competitively 'sponging' miR-342-3p.

Long non-coding RNA H19 regulates FOXM1 expression by competitively binding endogenous miR-342-3p in gallbladder cancer

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

Taken together, our research indicated an H19-miR138-HMGA1 pathway in regulating the migration and invasion of colon cancer, providing new insight for treatment of colon cancer.

H19 promotes the migration and invasion of colon cancer by sponging miR-138 to upregulate the expression of HMGA1

Transcriptional misregulation in cancer

Mechanisticlly, we demonstrated that H19 functions as a competing endogenous RNA (ceRNA) to sponge miRNA let-7a, leading to an increase in a let-7a target, the key regulator of tumor metastasis HMGA2, which is enriched in TSCC tissues and cell lines. Intriguingly, inhibition of let-7a significantly rescued short hairpin H19 (shH19) induced decrease of TSCC migration and invasion. These findings revealed that H19/let-7a/HMGA2/EMT axis plays a critical role in the regulation of TSCC migration and invasion, which may provide a new therapeutic target for TSCC cancers.

H19 facilitates tongue squamous cell carcinoma migration and invasion via sponging miR-let-7.

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

In addition, miR-140 dependent inhibitor of apoptosis-stimulating protein of p53 (iASPP) regulation was required in H19 induced glioma cell growth.

The lncRNA H19 interacts with miR-140 to modulate glioma growth by targeting iASPP

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

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.

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.

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

Meanwhile PTEN is an advantageous factor to affect H19 expression, through attenuating Hif-1α stability. Hif-1α also positively correlates with H19 in human glioblastoma samples depending on PTEN status. ChIP and luciferase reporter assays showed that Hif-1α induced H19 transcription through directly binding to the H19 promoter. Furthermore, Hif-1α upregulated specific protein 1 (SP1) expression in glioblastomas cells in vitro and in vivo, and SP1 also strongly interacted with the H19 promoter to promote H19 expression under hypoxia. We also showed that H19 acts as a molecular sponge that binds miR-181d, relieving inhibition of β-catenin expression.

Hypoxia induces H19 expression through direct and indirect Hif-1α activity, promoting oncogenic effects in glioblastoma

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

Amphetamine addiction

Remarkably, SIRT1 was confirmed as a direct target of miR-138-5p in cervical cancer and miR-138-5p exerted the tumor suppressed functions by suppressing SIRT1 expression.

Decreased Expression of MiR-138-5p by LncRNA H19 in Cervical Cancer Promotes Tumor Proliferation.

H19 suppressed miR-19b expression and miR-19b targeted Sox6, which inhibited cell proliferation and promoted apoptosis in P19CL6 cells during late-stage cardiac differentiation.

Downregulation of long non-coding RNA H19 promotes P19CL6 cells proliferation and inhibits apoptosis during late-stage cardiac differentiation via miR-19b-modulated Sox6

H19 suppressed miR-19b expression and miR-19b targeted Sox6, which inhibited cell proliferation and promoted apoptosis in P19CL6 cells during late-stage cardiac differentiation.

Downregulation of long non-coding RNA H19 promotes P19CL6 cells proliferation and inhibits apoptosis during late-stage cardiac differentiation via miR-19b-modulated Sox6

H19 acted as a sponge for miR-139 and H19 knockdown aggravated hypoxia-induced injury by up-regulating miR-139. Sox8 was identified as a target of miR-139, and its expression was negatively regulated by miR-139. The mechanistic studies revealed that overexpression of Sox8 might decrease hypoxia-induced cell injury by activating the PI3K/AKT/mTOR pathway and MAPK.

Long Non-Coding RNA H19 Protects H9c2 Cells against Hypoxia-Induced Injury by Targeting MicroRNA-139

Hippo signaling pathway；MAPK signaling pathway；Cytokine-cytokine receptor interaction；Cell cycle；Endocytosis；TGF-beta signaling pathway；Renal cell carcinoma；Hypertrophic cardiomyopathy (HCM)；Chronic myeloid leukemia；Toxoplasmosis；Pathways in cancer；Osteoclast differentiation；HTLV-I infection；Proteoglycans in cancer；Intestinal immune network for IgA production；Rheumatoid arthritis；Dilated cardiomyopathy；Hepatitis B；Pancreatic cancer；Leishmaniasis；Tuberculosis；Chagas disease (American trypanosomiasis)；Colorectal cancer； Malaria

Furthermore, miR-29b-3p directly suppressed the expression of TGF-β1 and type I collagen, thereby forming a novel regulatory feedback loop between H19 and TGF-β1 to mediate tenogenic differentiation.

Long noncoding RNA H19 accelerates tenogenic differentiation and promotes tendon healing through targeting miR-29b-3p and activating TGF-β1 signaling

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

Knockdown of H19 also decreased the VASH2 expression by up-regulating miR-29a.

Long non-coding RNA H19 regulates glioma angiogenesis and the biological behavior of glioma-associated endothelial cells by inhibiting microRNA-29a

Knockdown of H19 also decreased the VASH2 expression by up-regulating miR-29a.

Long non-coding RNA H19 regulates glioma angiogenesis and the biological behavior of glioma-associated endothelial cells by inhibiting microRNA-29a

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

Adherens junction；Tight junction

H19 antagonized the function of miR-17-5p on upregulation of its target YES1 and inhibited miR-17-5p-induced cell cycle progression.

Long noncoding RNA H19 competitively binds miR-17-5p to regulate YES1 expression in thyroid cancer

Transcriptional misregulation in cancer

Furthermore, by using bioinformatics study and RNA immunoprecipitation combined with luciferase reporter assays, we demonstrated that H19 functioned as a competing endogenous RNA (ceRNA) for miR-138 and miR-200a, antagonized their functions and led to the de-repression of their endogenous targets Vimentin, ZEB1, and ZEB2, all of which were core marker genes for mesenchymal cells.

The lncRNA H19 promotes epithelial to mesenchymal transition by functioning as miRNA sponges in colorectal cancer

Transcriptional misregulation in cancer

MiR-141 could also regulate H19 target genes and miR-141 inhibitor restores H19 siRNA function, while H19 regulates miR-141 target gene ZEB1.

The Interaction Between MiR-141 and lncRNA-H19 in Regulating Cell Proliferation and Migration in Gastric Cancer

Transcriptional misregulation in cancer

Furthermore, we showed that H19 promotes metastasis through upregulation of ZEB1 and ZEB2 by competitively binding the miR-200 family.

H19 Functions as a ceRNA in Promoting Metastasis Through Decreasing miR-200s Activity in Osteosarcoma

Transcriptional misregulation in cancer

Furthermore, by using bioinformatics study and RNA immunoprecipitation combined with luciferase reporter assays, we demonstrated that H19 functioned as a competing endogenous RNA (ceRNA) for miR-138 and miR-200a, antagonized their functions and led to the de-repression of their endogenous targets Vimentin, ZEB1, and ZEB2, all of which were core marker genes for mesenchymal cells.

The lncRNA H19 promotes epithelial to mesenchymal transition by functioning as miRNA sponges in colorectal cancer

Transcriptional misregulation in cancer

Furthermore, we showed that H19 promotes metastasis through upregulation of ZEB1 and ZEB2 by competitively binding the miR-200 family.

H19 Functions as a ceRNA in Promoting Metastasis Through Decreasing miR-200s Activity in Osteosarcoma

Transcriptional misregulation in cancer

Furthermore, we showed that H19 promotes metastasis through upregulation of ZEB1 and ZEB2 by competitively binding the miR-200 family.

H19 Functions as a ceRNA in Promoting Metastasis Through Decreasing miR-200s Activity in Osteosarcoma

Transcriptional misregulation in cancer

Furthermore, we showed that H19 promotes metastasis through upregulation of ZEB1 and ZEB2 by competitively binding the miR-200 family.

H19 Functions as a ceRNA in Promoting Metastasis Through Decreasing miR-200s Activity in Osteosarcoma

Furthermore, by using bioinformatics study and RNA immunoprecipitation combined with luciferase reporter assays, we demonstrated that H19 functioned as a competing endogenous RNA (ceRNA) for miR-138 and miR-200a, antagonized their functions and led to the de-repression of their endogenous targets Vimentin, ZEB1, and ZEB2, all of which were core marker genes for mesenchymal cells.

The lncRNA H19 promotes epithelial to mesenchymal transition by functioning as miRNA sponges in colorectal cancer

Furthermore, we showed that H19 promotes metastasis through upregulation of ZEB1 and ZEB2 by competitively binding the miR-200 family.

H19 Functions as a ceRNA in Promoting Metastasis Through Decreasing miR-200s Activity in Osteosarcoma

Furthermore, by using bioinformatics study and RNA immunoprecipitation combined with luciferase reporter assays, we demonstrated that H19 functioned as a competing endogenous RNA (ceRNA) for miR-138 and miR-200a, antagonized their functions and led to the de-repression of their endogenous targets Vimentin, ZEB1, and ZEB2, all of which were core marker genes for mesenchymal cells.

The lncRNA H19 promotes epithelial to mesenchymal transition by functioning as miRNA sponges in colorectal cancer

Furthermore, we showed that H19 promotes metastasis through upregulation of ZEB1 and ZEB2 by competitively binding the miR-200 family.

H19 Functions as a ceRNA in Promoting Metastasis Through Decreasing miR-200s Activity in Osteosarcoma

Furthermore, we showed that H19 promotes metastasis through upregulation of ZEB1 and ZEB2 by competitively binding the miR-200 family.

H19 Functions as a ceRNA in Promoting Metastasis Through Decreasing miR-200s Activity in Osteosarcoma

Furthermore, we showed that H19 promotes metastasis through upregulation of ZEB1 and ZEB2 by competitively binding the miR-200 family.

H19 Functions as a ceRNA in Promoting Metastasis Through Decreasing miR-200s Activity in Osteosarcoma