ncRNA-regulated immune response and its role in inflammatory lung diseases

Xie, Na; Liu, Gang

doi:10.1152/ajplung.00286.2015

Cited by 29 publications

(24 citation statements)

References 128 publications

(204 reference statements)

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“…The regulation of macrophage activation has been under extensive investigation, particularly at transcriptional and epigenetic levels (1). In the past decade, it has been increasingly clear that small ncRNAs, e.g., miRs, also play a crucial role in this process (11). A number of miRs have since been found to be intrinsically involved in a variety of pathogeneses through regulating macrophage activation (11).…”

Section: Discussionmentioning

confidence: 99%

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Long noncoding RNA Malat1 regulates differential activation of macrophages and response to lung injury

et al. 2019

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Section: Discussionmentioning

confidence: 99%

“…(ncRNAs), in these regulatory events. While there is plenty of evidence showing that small ncRNAs, such as microRNAs (miRs), participate in macrophage activation by targeting various mediators (10,11), it remains far less clear if, or how, long ncRNAs (lncRNAs) regulate this process.…”

Section: Introductionmentioning

confidence: 99%

Long noncoding RNA Malat1 regulates differential activation of macrophages and response to lung injury

et al. 2019

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“…Because of not coding, ncRNAs were previously known as junk RNAs. However, increasing evidence shows that ncRNAs play important regulatory roles in many biological and pathological processes, such as inflammation, viral infection, and apoptosis [6][7][8][9][10][11][12][13][14][15]. We previously reported that TGEV infection led to 21 differentially expressed miRNAs, among which miR-4331 inhibited transcription of TGEV gene7 via targeting CDCA7 [16], and miR-27b functioned as a negative regulator during TGEV-induced apoptosis [17].…”

Section: Introductionmentioning

confidence: 99%

Differentially expressed non-coding RNAs induced by transmissible gastroenteritis virus potentially regulate inflammation and NF-κB pathway in porcine intestinal epithelial cell line

Zhao

Zhang

et al. 2018

BMC Genomics

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BackgroundTransmissible gastroenteritis virus (TGEV) infection can activate NF-κB pathway in porcine intestinal epithelial cells and result in severe inflammation. Non-coding RNAs (ncRNAs) are not translated into proteins and play an important role in many biological and pathological processes such as inflammation, viral infection, and mitochondrial damage. However, whether ncRNAs participate in TGEV-induced inflammation in porcine intestinal epithelial cells is largely unknown.ResultsIn this study, the next-generation sequencing (NGS) technology was used to analyze the profiles of mRNAs, miRNAs, and circRNAs in Mock- and TGEV-infected intestinal porcine epithelial cell-jejunum 2 (IPEC-J2) cell line. A total of 523 mRNAs, 65 microRNAs (miRNAs), and 123 circular RNAs (circRNAs) were differentially expressed. Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis showed differentially expressed mRNAs were linked to inflammation-related pathways, including NF-κB, Toll-like receptor, NOD-like receptor, Jak-STAT, TNF, and RIG-I-like receptor pathways. The interactions among mRNA, miRNA, and circRNA were analyzed. The data showed that ssc_circ_009380 and miR-22 might have interaction relationship. Dual-luciferase reporter assay confirmed that miR-22 directly bound to ssc_circ_009380. We also observed that overexpression of miR-22 led to a reduction of p-IκB-α and accumulation of p65 in nucleus in TGEV-infected IPEC-J2 cells. In contrast, inhibition of miR-22 had the opposite effects. Moreover, silencing of ssc_circ_009380 inhibited accumulation of p65 in nucleus and phosphorylation of IκB-α.ConclusionsThe data revealed that differentially expressed mRNAs and ncRNAs were primarily enriched in inflammation-related pathways and ssc_circ_009380 promoted activation of NF-κB pathway by binding miR-22 during TGEV-induced inflammation.Electronic supplementary materialThe online version of this article (10.1186/s12864-018-5128-5) contains supplementary material, which is available to authorized users.

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“…For xenograft assays, we injected 1×10 6 modi ed (sh-circRNA, sh-circRNA + miR-519 inhibitor, or sh-circRNA + SMOC2) or control PANC-1 cells subcutaneously into male nude mice (Chinese Science Academy) in the right side. We measured tumor volumes (length × width 2 × 0.5) at the indicated time points, and excised tumors 4 weeks after injection.…”

Section: Animal Studiesmentioning

confidence: 99%

“…It is already known that ncRNA contributes to a large amount of cellular RNAs, making at least 90% of human RNAs [5]. Former studies have shown that ncRNAs, like proteins, act as underlying factors in various cellular processes, including cell migration, proliferation, apoptosis, chemoresistance, angiogenesis, and the immune response [6,7]. CircRNAs are considered as essential human disease regulators as well as biomarkers in many kinds of malignancies such like PC.…”

Section: Introductionmentioning

confidence: 99%

Knockdown of hsa_circ_0074298 suppressed the progression of pancreatic cancer by targeting the miR-519/SMOC2 axis

Chen

Wang

et al. 2020

Preprint

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BACKGROUND: Pancreatic cancer (PC) is among the most malignant tumors in the digestive system because of its fast progression, metastasis, as well as its resistance to chemotherapy. Former studies found that circRNAs that were differentially expressed were correlated with progression and gemcitabine (GEM)-resistance in PC, and hsa_circ_0074298 aberrant expression played a role in PC progression, but the regulatory mechanism was unclear. METHODS: RT-qPCR was used to detect hsa_circ_0074298 expression in PC cell lines. CCK8, colony formation, and Transwell assays were used to evaluate the effect of hsa_circ_0074298 on PC cell migration and proliferation. Bioinformatics and luciferase reporter experiments were used to characterize the regulatory mechanism. Nude mouse xenografts were generated to examine the effect of hsa_circ_0074298 on tumor growth. RESULTS: The present study showed that hsa_circ_0074298 expression increased significantly in both PC cell lines and PC tissues. Downregulation of hsa_circ_0074298 caused a significant decrease in PC cell proliferation and in nude mouse xenograft growth. Hsa_circ_0074298 silencing also increased chemotherapy sensitivity to GEM. Bioinformatics analysis indicated that hsa_circ_0074298 was a miR-519 sponge and that the SMOC2 gene was a miR-519 target. MiR-519 downregulation or SMOC2 overexpression restored cell proliferation, migration, and chemoresistance after hsa_circ_0074298 silencing. The dual luciferase reporter assay showed that hsa_circ_0074298 interacted with miR-519, and miR-519 binding to the SMOC2 3′-UTR then suppressed posttranscriptional SMOC2 expression. CONCLUSIONS: Taken together, hsa_circ_0074298 functioned as a tumor promoter through a novel miR-519/SMOC2 axis, highlighting its possibility as a potential therapy for PC.

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ncRNA-regulated immune response and its role in inflammatory lung diseases

Cited by 29 publications

References 128 publications

Long noncoding RNA Malat1 regulates differential activation of macrophages and response to lung injury

Long noncoding RNA Malat1 regulates differential activation of macrophages and response to lung injury

Differentially expressed non-coding RNAs induced by transmissible gastroenteritis virus potentially regulate inflammation and NF-κB pathway in porcine intestinal epithelial cell line

Knockdown of hsa_circ_0074298 suppressed the progression of pancreatic cancer by targeting the miR-519/SMOC2 axis

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