LncRNA H19 over-expression inhibited Th17 cell differentiation to relieve endometriosis through miR-342-3p/IER3 pathway

Liu, Zheying; Liu, Liya; Zhong, Yun; Cai, Mingbo; Gao, Junbi; Tan, Chaoyue; Han, Xing; Guo, Ruixia; Liang, Han

doi:10.1186/s13578-019-0346-3

Cited by 44 publications

(34 citation statements)

References 26 publications

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“…This is accompanied with an increase in miR-342-3p levels. This miRNA binds with the 3 ′ UTR of IER3, thus inhibiting its expression (93). IER3 participates in proteasomal degradation of IF-1.…”

Section: Figure 1 | (A)mentioning

confidence: 99%

“…In addition, Xu et al have demonstrated the role of the estrogen-modulated H19/ACTA2/miR-216a-5p axis in the regulation of invasion and migration of eutopic endometrial stromal cells in subjects with endometriosis ( 78 ). Liu et al have reported the significance of H19/miR-342-3p/IER3 axis in suppression of Th17 cell differentiation and decreasing the risk of endometriosis ( 93 ). A recent high throughput study of RNA profile of the ectopic and eutopic endometrium of patients has led to construction of the ceRNA network.…”

Section: Interaction Between Mirnas and Lncrnas In The Pathogenesis Omentioning

confidence: 99%

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Role of Non-coding RNAs in the Pathogenesis of Endometriosis

2020

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Endometriosis is a disorder characterized by the presence of endometrial glands and stroma like lesions outside of the uterus. Although several hypothesis have tried to explain the underlying cause of endometriosis, yet the main cause remained obscure. Recent studies have shown contribution of non-coding RNAs in the pathogenesis of endometriosis. Two classes of these transcripts namely long non-coding RNAs (lncRNAs) and microRNAs (miRNAs) have mostly attracted attention of researchers. Several studies have reported aberrant expression of these transcripts in affected tissues from patients as well as animal models. Modulation of important signaling pathways such as PI3K/AKT, P38-MAPK, ERK1/2-MAPK and Wnt-β catenin by miRNAs and lncRNAs have potentiated these molecules as biomarkers or therapeutic agents in endometriosis. Single nucleotide polymorphisms with miR-126, miR-143 and miR-146b have been associated with risk of endometriosis. Moreover, miRNAs and lncRNAs control inflammatory responses, cell proliferation, angiogenesis and tissue remodeling, thus understanding the role of these transcripts in endometriosis is a possible way to develop novel diagnostic tests and therapeutic targets for this disorder.

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Section: Figure 1 | (A)mentioning

confidence: 99%

Section: Interaction Between Mirnas and Lncrnas In The Pathogenesis Omentioning

confidence: 99%

Role of Non-coding RNAs in the Pathogenesis of Endometriosis

2020

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“…LncRNAs, a class of transcripts longer than 200 nucleotides with a limited or without protein-coding function, are involved in many diseases owing their modulating effect toward diverse biological processes, such as cell proliferation, apoptosis, and differentiation 17 . More importantly, many lncRNAs, such as lncRNA MEG3, lncRNA NEAT1, and lncRNA H19, have been proven to be tightly linked to Th7 cell differentiation 18 – 20 . Colorectal neoplasia differentially expressed (CRNDE), an lncRNA located on chromosome 16, is highly expressed in multiple cancers, and it plays indispensable roles in the development of different types of cancer, including CRC 21 .…”

Section: Introductionmentioning

confidence: 99%

Tumor exosome promotes Th17 cell differentiation by transmitting the lncRNA CRNDE-h in colorectal cancer

et al. 2021

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The T helper 17 (Th17) cells in tumor microenvironment play an important role in colorectal cancer (CRC) progression. This study investigated the mechanism of Th17 cell differentiation in CRC with a focus on the role of tumor exosome-transmitted long noncoding RNA (lncRNA). Exosomes were isolated from the CRC cells and serum of CRC patients. The role and mechanism of the lncRNA CRNDE-h transmitted by CRC exosomes in Th17 cell differentiation were assessed by using various molecular biological methods. The serum exosomal CRNDE-h level was positively correlated with the proportion of Th17 cells in the tumor-infiltrating T cells in CRC patients. CRC exosomes contained abundant CRNDE-h and transmitted them to CD4+ T cells to increase the Th17 cell proportion, RORγt expression, and IL-17 promoter activity. The underlying mechanism is that, CRNDE-h bound to the PPXY motif of RORγt and impeded the ubiquitination and degradation of RORγt by inhibiting its binding with the E3 ubiquitin ligase Itch. The in vivo experiments confirmed that the targeted silence of CRNDE-h in CD4+ T cells attenuated the CRC tumor growth in mice. The present findings demonstrated that the tumor exosome transmitted CRNDE-h promoted Th17 cell differentiation by inhibiting the Itch-mediated ubiquitination and degradation of RORγt in CRC, expanding our understanding of Th17 cell differentiation in CRC.

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“…Previous studies have shown that lncRNA H19 is involved in the regulation of expression of many miRNAs. [21][22][23][24] Liu et al 25 stated that up-regulated lncRNA H19 participates in the regulation of proliferation and apoptosis of endometrial stromal cells (ESCs), so lncRNA H19 may be related to adenomyosis.…”

Section: Introductionmentioning

confidence: 99%

<p>Levonorgestrel Ameliorates Adenomyosis via lncRNA H19/miR-17/TLR4 Pathway</p>

Liang¹,

Zhang²,

Wang³

et al. 2020

DDDT

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To explore the mechanism of levonorgestrel (LNG)-ameliorating adenomyosis through long non-coding RNA H19 (lncRNA H19)/miR-17/Toll-like receptor 4 (TLR4) pathway. Patients and Methods: A total of 71 cases of adenomyosis and 54 cases of normal endometrium were sampled. Quantitative polymerase chain reaction (qPCR) was employed to quantify lncRNA H19, miR-17, and TLR4 mRNA, while Western blot (WB) was used to quantify TLR4 protein. Effects of LNG on normal endometrial stromal cells (ESCs) were evaluated. Suppression/over-expression vectors of lncRNA H19, miR-17, and TLR4 were constructed to observe their effects on ESCs. Results: MiR-17 and TLR4 mRNA were up-regulated and lncRNA H19 was downregulated in adenomyosis. After LNG treatment, lncRNA H19 was up-regulated while miR-17 and TLR4 were down-regulated. LNG, up-regulation of lncRNA H19, and downregulation of miR-17 and TLR4 portend increased apoptosis, G1-arrested cells, as well as inhibited inflammation. Dual-luciferase reporter (DLR) assay conformed the targeting relation of lncRNA H19/miR-17/TLR4 pathway. Conclusion: LNG ameliorates adenomyosis via lncRNA H19/miR-17/TLR4 pathway.

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LncRNA H19 over-expression inhibited Th17 cell differentiation to relieve endometriosis through miR-342-3p/IER3 pathway

Cited by 44 publications

References 26 publications

Role of Non-coding RNAs in the Pathogenesis of Endometriosis

Role of Non-coding RNAs in the Pathogenesis of Endometriosis

Tumor exosome promotes Th17 cell differentiation by transmitting the lncRNA CRNDE-h in colorectal cancer

<p>Levonorgestrel Ameliorates Adenomyosis via lncRNA H19/miR-17/TLR4 Pathway</p>

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