Overexpression of long non-coding RNA H19 promotes invasion and autophagy via the PI3K/AKT/mTOR pathways in trophoblast cells

Xu, Jin; Xia, Yaoyao; Zhang, Helong; Guo, Haibin; Feng, Ke; Zhang, Cuilian

doi:10.1016/j.biopha.2018.02.134

Cited by 70 publications

(59 citation statements)

References 38 publications

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“…Moreover, they observed that the overexpression H19 initiated autophagy in trophoblast cells. 21 Nevertheless, there is no published report on the association between H19 polymorphisms and mRNA expression of this gene and our attempt is the first study in this topic.…”

Section: Discussionmentioning

confidence: 85%

“…Recently, Xu et al evaluated the placental H19 expression in PE patients and healthy pregnant women ( n = 20 for each group); they found higher level of H19 in the placenta tissues of PE and non‐preeclamptic women. Moreover, they observed that the overexpression H19 initiated autophagy in trophoblast cells …”

Section: Discussionmentioning

confidence: 99%

“…Increased levels of H19 expression in embryonic tissues result in the regulation of embryonic growth and development and placental cytotrophoblast differentiation . The recent literature has reported the overexpression of lncRNA‐H19 in preeclamptic placentas compared to healthy controls . It has been shown that H19 acts as a primary microRNA precursor, and H19 expression regulates specific mRNAs via post‐transcription .…”

Section: Introductionmentioning

confidence: 99%

“…19,20 The recent literature has reported the overexpression of lncRNA-H19 in preeclamptic placentas compared to healthy controls. 21 It has been shown that H19 acts as a primary microRNA precursor, and H19 expression regulates specific mRNAs via post-transcription. 22 The effect of genetic mutation and polymorphisms on lncRNA structure, stability, expression, and thereby, its association with disease development are illustrated in previous studies.…”

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confidence: 99%

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The effects of placental long noncoding RNA H19 polymorphisms and promoter methylation on H19 expression in association with preeclampsia susceptibility

et al. 2019

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The effect of DNA methylation on gene expression triggered it as a susceptibility factor in various diseases including preeclampsia (PE). The pathogenesis of PE is closely associated with the methylation status and genetic variants of relevant genes. Therefore, the aim of the study was to investigate the possible impacts of the placental DNA methylation and rs3741219, rs217727, and rs2107425 polymorphisms of the H19 gene on the PE susceptibility as well as the its mRNA expression. Moreover, eight haplotypes of three loci in the H19 gene were analyzed. In this case‐control study, the placentas of 107 preeclamptic and 113 non‐preeclamptic women were collected after delivery. The methylation status was assessed by methylation‐specific polymerase chain reaction (PCR). The H19 polymorphisms were genotyped using polymerase chain reaction‐restriction fragment length polymorphism or amplification refractory mutation system‐polymerase chain reaction methods. The quantitative real time PCR was used for mRNA expression assay. The placental H19 rs3741219 and rs2107425 polymorphisms were not associated with PE. However, H19 rs217727CT and TT genotypes might be associated with a 9.2‐ and 17.7‐fold increased risk of PE, respectively. The Trs3741219 Crs217727 Crs2107425 and Trs3741219 Crs217727 Trs2107425 haplotypes were significantly lower, whereas the Trs3741219 Trs217727 Crs2107425 and Crs3741219 Trs217727 Crs2107425 haplotypes were significantly higher in PE women. Promoter but not upstream region hypermethylation of H19 gene could be led to decreased risk of PE (MM vs. UM + UU). No significant difference was observed in the placental mRNA expression between two groups. The H19 expression was significantly higher in women with unmethylated (UU), compared to methylated promoter (MM). The H19 expression was 17‐ and 15‐fold higher in H19‐rs2107425 CC and CT genotypes in PE women. In conclusion, the H19 rs2107425 polymorphism was associated with a higher risk of PE and increased H19 mRNA expression. The promoter hypermethylation of H19 gene was associated with a lower risk of PE and decreased H19 mRNA expression.

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Section: Discussionmentioning

confidence: 85%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

mentioning

confidence: 99%

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The effects of placental long noncoding RNA H19 polymorphisms and promoter methylation on H19 expression in association with preeclampsia susceptibility

et al. 2019

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“…To unravel the mechanisms of CUL4B regulating autophagy in DLBCL cells, possible regulatory pathways were evaluated. Several signaling pathways have been demonstrated to participate in autophagy regulation in solid cancers [25][26][27][28], but the mediated mechanisms in DLBCL still remains unknown. Previous research regarded the regulating pathways, mainly PI3K/AKT/mTOR and JNK signaling pathways, as the targeted treatment for DLBCL due to their positive regulation in further promotion of cell survival, proliferation, and drug resistance [2,29,30].…”

Section: Role Of Cul4b In Autophagy and Related Mechanismmentioning

confidence: 99%

CUL4B regulates autophagy via JNK signaling in diffuse large B-cell lymphoma

Zhou

Zhang

et al. 2019

Cell Cycle

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Aberrant expression of CUL4B was identified in various types of solid cancers. Cumulative evidences support the oncogenic role of CUL4B in cancers, including regulation of cell proliferation and signal transduction. However, its clinical value and potential pathogenic mechanism in diffuse large B-cell lymphoma (DLBCL) have not been described previously. Therefore, we hypothesize that overexpressed CUL4B may contribute to the pathogenesis of DLBCL. The aim of this study is to assess the expression and the biological function of CUL4B in DLBCL progression. In our study, CUL4B overexpression was observed in DLBCL tissues, and its upregulation was closely associated with poor prognosis in patients. Furthermore, the functional roles of CUL4B was detected both in vitro and in vivo. We demonstrated that silencing CUL4B could not only induce cell proliferation inhibition, cell cycle arrest, and motility attenuation of DLBCL cells in vitro, but also decrease tumor growth in DLBCL xenografts mice. In addition, we identified that CUL4B may act as a potent inductor of JNK phosphorylation in regulation of autophagy. Our findings demonstrated a significant role of CUL4B in the development and progression of DLBCL. CUL4B may act as a useful biomarker and a novel therapeutic target in DLBCL. ARTICLE HISTORY

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Long noncoding RNA H19 in ovarian biology and placenta development

Adu‐Gyamfi,

Cheeran,

Salamah

et al. 2024

Cell Biochemistry & Function

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As the first long noncoding RNA to be discovered, H19 has gained substantial attention as a key regulator of several biological processes and its roles in female reproductive biology are gradually getting revealed. Herein, we have summarized the current evidence regarding H19 expression pattern and involvement in the developmental and pathological processes associated with the ovary and the placenta. The findings indicate that within the ovaries, H19 is expressed in the antral and cystic atretic follicles as well as in the corpora lutea but absent in the primordial, primary, and secondary follicles. Its normal expression promotes the maturation of antral follicles and prevents their premature selection for the ovulatory journey while its aberrant induction promotes polycystic ovary syndrome development and ovarian cancer metastasis. In the placenta, H19 is highly expressed in the cytotrophoblasts and extravillous trophoblasts but weakly expressed in the syncytiotrophoblast layer and potentially controls trophoblast cell fate decisions during placenta development. Abnormal expression of H19 is observed in the placental villi of pregnancies affected by pre‐eclampsia and fetal growth restriction. Therefore, dysregulated H19 is a candidate biomarker and therapeutic target for the mitigation of ovarian and placenta‐associated diseases.

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Overexpression of long non-coding RNA H19 promotes invasion and autophagy via the PI3K/AKT/mTOR pathways in trophoblast cells

Cited by 70 publications

References 38 publications

The effects of placental long noncoding RNA H19 polymorphisms and promoter methylation on H19 expression in association with preeclampsia susceptibility

The effects of placental long noncoding RNA H19 polymorphisms and promoter methylation on H19 expression in association with preeclampsia susceptibility

CUL4B regulates autophagy via JNK signaling in diffuse large B-cell lymphoma

Long noncoding RNA H19 in ovarian biology and placenta development

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