Long non-coding RNA H19 mediates mechanical tension-induced osteogenesis of bone marrow mesenchymal stem cells via FAK by sponging miR-138

Wu, Jiajing; Zhao, Jing; Sun, Lian; Pan, Yongchu; Wang, Hua; Zhang, Weibing

doi:10.1016/j.bone.2017.12.013

Cited by 109 publications

(98 citation statements)

References 35 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In addition, β1 integrin promoted the apoptosis of HCC cells through the FAK/Akt signaling. 25 In this study, we investigated the role of HBV infection in the tumorigenesis of hepatoblastoma by modulating the two possible signaling pathways, that is, HBV/HBX/HIF1A/H19/miR-675/FADD/caspase-3 and HBV/HBX/HIF1A/H19/miR-138/PTK2/FAK. 19 Apoptosis can be induced via death receptors (DRs), including tumor necrosis factor receptor-1 (TNF-R1) and Fas.…”

Section: Introductionmentioning

confidence: 99%

RETRACTED: H19 suppresses the growth of hepatoblastoma cells by promoting their apoptosis via the signaling pathways of miR‐675/FADD and miR‐138/PTK2

Zhang

et al. 2018

J of Cellular Biochemistry

View full text Add to dashboard Cite

Background The objective of this study was to clarify the molecular pathways involved in hepatitis B virus (HBV)‐induced hepatoblastoma. Method The expression of factors in different signaling pathways (H19, miR‐675, miR‐138, protein tyrosine kinase 2 [PTK2], fas‐associated death domain [FADD], hypoxia‐inducible factor 1‐alpha [HIFIA], focal adhesion kinase [FAK], caspase‐8, and caspase‐3) was compared between HBV (+) and HBV (−) groups using quantitative real‐time polymerase chain reaction and Western blot analysis. Subsequently, immunohistochemistry (IHC) and TdT‐mediated dUTP Nick‐End Labeling (TUNEL) assays were used to verify the expression of above proteins in HBV (+) and HBV (−) groups. Computational analysis was conducted to predict the target genes of miR‐675 and miR‐138, whose regulatory relationships were then clarified using luciferase assays and cell transfection studies. Result The expression of H19, miR‐675, PTK2, HIFIA, and FAK was increased in the HBV (+) group, while the expression of miR‐138, FADD, caspase‐8, and caspase‐3 was decreased in the HBV (+) group. FADD and PTK2 were identified as target genes of miR‐675 and miR‐138, respectively. In addition, miR‐675 was upregulated while miR‐138 was downregulated by X protein (HBx). Conclusion In summary, the results of this study revealed the molecular pathways involved in HBV‐induced hepatoblastoma. In the presence of HBV, HBX upregulated the expression of H19 through HIFIA. Consecutively, overexpressed H19 upregulated the expression of PTK2 via targeting miR‐138 and downregulated the expression of FADD via targeting miR‐675. Finally, increased expression of PTK2 and reduced expression of FADD both led to the inhibition of cell apoptosis, thus promoting the tumorigenesis of hepatoblastoma.

show abstract

Section: Introductionmentioning

confidence: 99%

RETRACTED: H19 suppresses the growth of hepatoblastoma cells by promoting their apoptosis via the signaling pathways of miR‐675/FADD and miR‐138/PTK2

Zhang

et al. 2018

J of Cellular Biochemistry

View full text Add to dashboard Cite

show abstract

“…J. Wu et al (2018) showed that H19 deficiency suppressed tension-induced osteogenic differentiation in BMSCs. Y. Wang et al…”

Section: Discussionmentioning

confidence: 99%

H19 and Foxc2 synergistically promotes osteogenic differentiation of BMSCs via Wnt‐β‐catenin pathway

Zhou

Liu

et al. 2019

Journal Cellular Physiology

View full text Add to dashboard Cite

Objective To investigate the mechanism of H19 on the osteogenic differentiation of bone marrow mesenchymal stem cells (BMSCs). Methods Ovariectomized (OVX) mouse model was established. RNA immunoprecipitation and RNA pull‐down assays were performed to determine the correlation between H19 and forkhead box C2 (Foxc2). Chromatin immunoprecipitation assay was used to identify whether Foxc2 binds to the Wnt4 promoter region. Molecules expressions were measured by quantitative real‐time polymerase chain reaction and western blot. Results We found that H19 expression was reduced in the serum of patients with postmenopausal osteoporosis and BMSCs of OVX mice, and overexpression of H19 promoted osteogenic differentiation of BMSCs. Additionally, Foxc2 could bind to the Wnt4 promoter and promote its transcription. We also showed that H19 could bind to Foxc2, and H19/Foxc2 regulated Wnt promoter expression in a synergistic fashion, and H19/Foxc2 regulated osteogenic differentiation of BMSCs through Wnt‐β‐catenin pathway. Conclusion H19 and Foxc2 synergistically promoted osteogenic differentiation of BMSCs via Wnt‐β‐catenin pathway.

show abstract

“…Meanwhile, a mass of lncRNAs such as H19 and MEG3 had been reported to regulate the adipogenesis and osteogenesis in BMSCs (Wang et al, ; Zhuang et al, ). A considerable amount of evidence has identified that H19 stimulated osteogenic differentiation of mBMSC and suppressed adipogenic differentiation of mBMSCs (Huang et al, ; Wu et al, ). However, the regulatory mechanism of lncNRA H19/miR‐188 axis in mBMSCs remains unknown.…”

Section: Introductionmentioning

confidence: 99%

Long noncoding RNA H19 mediates LCoR to impact the osteogenic and adipogenic differentiation of mBMSCs in mice through sponging miR‐188

Wang

Liu

et al. 2018

Journal Cellular Physiology

View full text Add to dashboard Cite

The research aimed to examine the expression of lncRNA H19, miR-188, and LCoR in mouse bone marrow stromal stem cells (mBMSCs), and to investigate the regulatory mechanism of lncRNA H19/miR-188/LCoR in osteogenic and adipogenic differentiation of mBMSCs. The expression of miR-188 in mBMSCs and osteogenesis induced mBMSCs was detected by stem-loop RT-PCR, while the expression of H19 and LCoR in mBMSCs and adipogenesis induced mBMSCs was examined by qRT-PCR. Luciferase reporter assay verified the targeted relationship between miR-188 and H19 or LCoR. Cell proliferation ability was determined by MTT assay, while cell surface markers of mBMSCs were analyzed via flow cytometry. Alkaline phosphatase staining and Alizarin red staining was utilized to detect the osteogenic differentiation capability of mBMSCs, whereas Oil red O staining was applied to examine the ability of adipogenic differentiation of mBMSCs. The expression of miR-188 was lower in osteogenesis induced mBMSCs compared with normal mBMSCs, while H19 and LCoR were downregulated in adipogenic induced mBMSCs. Si-H19 could significantly increase the mRNA level of miR-188. Meanwhile, miR-188 directly regulated LCoR in mBMSCs. Overexpression of miR-188 and knockdown of LCoR suppressed osteogenic differentiation and induced adipogenic differentiation in mBMSCs. Long noncoding RNA H19 mediates LCoR to regulate the balance between osteogenic and adipogenic differentiation of mBMSCs in mice through sponging miR-188.

show abstract

Long non-coding RNA H19 mediates mechanical tension-induced osteogenesis of bone marrow mesenchymal stem cells via FAK by sponging miR-138

Cited by 109 publications

References 35 publications

RETRACTED: H19 suppresses the growth of hepatoblastoma cells by promoting their apoptosis via the signaling pathways of miR‐675/FADD and miR‐138/PTK2

RETRACTED: H19 suppresses the growth of hepatoblastoma cells by promoting their apoptosis via the signaling pathways of miR‐675/FADD and miR‐138/PTK2

H19 and Foxc2 synergistically promotes osteogenic differentiation of BMSCs via Wnt‐β‐catenin pathway

Long noncoding RNA H19 mediates LCoR to impact the osteogenic and adipogenic differentiation of mBMSCs in mice through sponging miR‐188

Contact Info

Product

Resources

About