circRNA Expression Pattern and circRNA–miRNA–mRNA Network in HCs, HSCs, and KCs of Murine Liver After Echinococcus multilocularis Infection

Liu, Tingli; Wang, Liqun; Li, Hong; Li, Yanping; Chen, Guoliang; Pu, Guiting; Guo, Xiaola; Zheng, Yadong; Bai, Xue; Luo, Xuenong

doi:10.3389/fvets.2022.825307

Cited by 2 publications

(3 citation statements)

References 30 publications

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“…As is known to all, circRNAs are rich in the binding sites of miRNA, which could interfere translation of mRNA, thereby participating in regulation of multifarious biological processes 35 . As an important miRNA, miR‐637 has been broadly reported in sundry cancers, including gastric cancer, 36 glioblastoma, 37 and papillary thyroid carcinoma 38 .…”

Section: Discussionmentioning

confidence: 99%

“…33 As is known to all, circRNAs are rich in the binding sites of miRNA, which could interfere translation of mRNA, thereby participating in regulation of multifarious biological processes. 35 As an important miRNA, miR-637 has been broadly reported in sundry cancers, including gastric cancer, 36 glioblastoma, 37 and papillary thyroid carcinoma. 38 Several researches demonstrated that miR-637 as a sponger to involve in modulating the effect of circRNAs on cancer cells proliferation, metastasis, and apoptosis.…”

Section: Knockdown Of Circ_0000877 Inhibited Nsclc Tumor Growth In Vivomentioning

confidence: 99%

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Circ_0000877 accelerates proliferation and immune escape of non‐small cell lung cancer cells by regulating microRNA‐637/E2F2 axis

Chen,

Li,

Chen

et al. 2024

Environmental Toxicology

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BackgroundRecently, circular RNA (circRNA) has become a vital targeted therapy gene for non‐small‐cell lung cancer (NSCLC) cells. CircRNA_0000877 (Circ_0000877) has been researched in diffuse large B‐cell lymphoma (DLBCL). However, whether circ_0000877 regulated NSCLC cell progression is still poorly investigated. The research attempted to investigate the influence of circ_0000877 in NSCLC.MethodsCirc_0000877 levels in NSCLC tissues and cell lines were determined applying RT‐qPCR. Cell functions were evaluated by CCK‐8, EdU, flow cytometry, ELISA, and western blot. Gene interactions were predicted by Cirular RNA interactome database and Target Scan website and certified by dual‐luciferase reporter, RIP, and RNA pull‐down assays. Finally, mice experimental model was established to explore the effects of circ_0000877 on tumor growth in vivo.ResultsThe elevated trend of circ_0000877 expression was discovered in NSCLC tissues compared to para‐carcinoma tissues. The clinicopathological data uncovered that up‐regulated circ_0000877 was linked to tumor size, differentiation, and TNM stages of NSCLC patients. Knockdown of circ_0000877 inhibited the proliferation, triggered apoptosis, and prohibited immune escape in NSCLC cells. It was certified that miR‐637 was directly interacted with circ_0000877 and targeted by E2F2. Overexpressed E2F2 strongly overturned the functions of circ_0000877 knockdown in NSCLC cells. Mice experimental data demonstrated that circ_0000877 knockdown suppressed tumor growth in vivo.ConclusionThe research demonstrated that circ_0000877 exhibited the promotive effect on NSCLC cells proliferation and immune escape by regulating miR‐637/E2F2 axis.

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Section: Discussionmentioning

confidence: 99%

Section: Knockdown Of Circ_0000877 Inhibited Nsclc Tumor Growth In Vivomentioning

confidence: 99%

Circ_0000877 accelerates proliferation and immune escape of non‐small cell lung cancer cells by regulating microRNA‐637/E2F2 axis

Chen,

Li,

Chen

et al. 2024

Environmental Toxicology

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“…The miRNA expression in HSCs after E. multilocularis infection was investigated using highthroughput sequencing [25]. Raw reads were generated subsequently, which were deposited in NCBI Sequence Read Archive (SRA) under accession number PRJNA732233.…”

Section: Identification Of Differentially Expressed Known Mirnasmentioning

confidence: 99%

mmu-miRNA-342-3p promotes hepatic stellate cell activation and hepatic fibrosis induced by Echinococcus multilocularis infection via targeting Zbtb7a

Cao¹,

Wang²,

Wu³

et al. 2023

PLoS Negl Trop Dis

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Liver fibrosis is one of the histopathological characters during Echinococcus multilocularis infection. The activation of hepatic stellate cells (HSCs) is a key event in the development of liver fibrosis. However, the molecular mechanism of HSC activation in the E. multilocularis infection-induced liver fibrosis remains largely unclear. Here, we reported that mmu-miR-342-3p was most dominantly expressed in HSCs and was upregulated in the HSCs in response to E. multilocularis infection. We further showed that mmu-miR-342-3p was able to bind to the 3’ UTR of the Zbtb7a gene and regulated its expression. Moreover, mmu-miR-342-3p expression was negatively correlated with its target gene Zbtb7a in HSCs during E. multilocularis infection. Knockdown of mmu-miR-342-3p promoted the expression of Gfap in the activated HSCs in vitro. In the E. multilocularis-infected mice, knockdown of mmu-miR-342-3p suppressed the expression of α-Sma, Col1α1, and TGF-β but promoted the expression of Gfap. Therefore, mmu-miR-342-3p is a key regulator for activation of HSCs, and inhibiting mmu-miR-342-3p to promote Zbtb7a-mediated TGF-β signaling in activated HSCs could be a novel strategy to treat liver fibrosis induced by E. multilocularis.

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circRNA Expression Pattern and circRNA–miRNA–mRNA Network in HCs, HSCs, and KCs of Murine Liver After Echinococcus multilocularis Infection

Cited by 2 publications

References 30 publications

Circ_0000877 accelerates proliferation and immune escape of non‐small cell lung cancer cells by regulating microRNA‐637/E2F2 axis

Circ_0000877 accelerates proliferation and immune escape of non‐small cell lung cancer cells by regulating microRNA‐637/E2F2 axis

mmu-miRNA-342-3p promotes hepatic stellate cell activation and hepatic fibrosis induced by Echinococcus multilocularis infection via targeting Zbtb7a

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