Functional diversity of long non-coding RNAs in immune regulation

Geng, Hua; Tan, Xiao Di

doi:10.1016/j.gendis.2016.01.004

Cited by 66 publications

(54 citation statements)

References 76 publications

(186 reference statements)

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“…Because the function of immune-related lncRNA has been discovered, lncRNA can interact with transcription factors and chromatin remodeling components (PRC2, WDR5). 47 A previous study from our laboratory demonstrated that the defect in SUV39H1/H3K9me3 is implicated in abnormal inflammation in COPD. 48 Thus, potential interactions of lnc-IL7R with SUV39H1 methyltransferase and other epigenetic regulators may be implicated in the regulatory mechanism, which warrants further elucidation.…”

Section: Discussionmentioning

confidence: 94%

Impaired lnc‐IL7R modulatory mechanism of Toll‐like receptors is associated with an exacerbator phenotype of chronic obstructive pulmonary disease

Feng

Chuang

et al. 2020

FASEB j.

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Patients with chronic obstructive pulmonary disease (COPD) are susceptible to bacterial infections, which worsen lung inflammation and contribute to lung function decline and acute exacerbation. Long noncoding (lnc) RNAs are emerging regulators of inflammation with unknown clinical relevance. Herein, we report that levels of the Toll‐like receptor (TLR)‐related lnc interleukin (IL) 7 receptor (IL7R) were significantly reduced in peripheral blood mononuclear cells from patients with COPD compared with those from normal controls, and the levels were correlated with pulmonary function. Moreover lnc‐IL7R levels were reduced in lavaged alveolar macrophages and primary human small airway epithelial cells (HSAEpCs) from patients with COPD. Lnc‐IL7R knockdown in primary human macrophages, HSAEpCs, and human pulmonary microvascular endothelial cells (HPMECs) significantly augmented the induction of proinflammatory mediators after TLR2/4 activation. By contrast, lnc‐IL7R overexpression attenuated inflammation after TLR2/4 activation. Similar results with lnc‐IL7R‐mediated inflammation were observed in COPD HSAEpCs. Mechanistically, lnc‐IL7R mediated a repressive chromatin state of the proinflammatory gene promoter as a result of decreased acetylation (H3K9ac) and increased methylation (H3K9me3 and H3K27me3). Plasma lnc‐IL7R levels were reduced in patients with COPD who experienced more acute exacerbation in the previous year. Notably, patients with lower lnc‐IL7R levels in the subsequent year had increased exacerbation risk. Low lnc‐IL7R expression in COPD may augment TLR2/4‐mediated inflammation and be associated with acute exacerbation.

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Section: Discussionmentioning

confidence: 94%

Impaired lnc‐IL7R modulatory mechanism of Toll‐like receptors is associated with an exacerbator phenotype of chronic obstructive pulmonary disease

Feng

Chuang

et al. 2020

FASEB j.

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“…FOXO1 suppressed cell metastasis by down-regulating AKT and inhibited lung cancer [16]. Hence, targeting lncRNAs could be considered as another approach to prevent and treat HCC [17][18][19][20]. According to previous study, it has been proved that LINC00668 is an oncogene in several cancers such as non-small-cell lung cancer [21] and gastric cancer then transferred to a polyvinylidene fluoride (PVDF) (Sigma-Aldrich).…”

Section: Introductionmentioning

confidence: 99%

LncRNA LINC00668 promotes cell proliferation, migration, invasion ability and EMT process in hepatocellular carcinoma by targeting miR-532-5p/YY1 axis

2020

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Liver cancer is now one of the most lethal and commonest cancers in the world, among which over 90% is hepatocellular carcinoma (HCC). Recent studies have confirmed long non-coding RNAs (lncRNAs) are implicated in carcinogenesis. It has been reported lncRNA LINC00668 serves as an oncogene in several cancers. However, the mechanism where LINC00668 regulates HCC is still unclear. qRT-PCR analysis was adopted to detect the expression of relative RNAs. Cytoplasmic and nuclear RNA fraction analysis was conducted to verify the underlying molecular mechanism. Cell colony formation was carried out to test cell colony formation ability and transwell assays were performed to testify cell migratory and invaded abilities. Relevant protein expression level was measured by Western blot assay. LINC00668 was significantly up-regulated in HCC tissues and cell lines. LINC00668 knockdown inhibited cell proliferative, migratory and invasion abilities and slowed down the epithelial–mesenchymal transition (EMT) process. Mechanistically, LINC00668 positively modulates the expression of YY1 by competitively binding to miR-532-5p. It was revealed that LINC00668 up-regulation accelerated cell proliferation and motility in HCC and suggested LINC00668 could be a potential therapeutic target for HCC.

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“…lncRNAs have low sequence conservation and mediate gene expression at post-transcriptional level through interaction with nucleic acids and proteins. And lncRNAs broadly participate in varied biological aspects, such as cell growth, differentiation, chromosome inactivation and even tumorigenesis [8][9][10][11]. In regard of cancer, an increasing amount of lncRNAs have been found to function as oncogenes or antioncogenes [12].…”

Section: Introductionmentioning

confidence: 99%

RETRACTED ARTICLE: Silence of lncRNA ANRIL represses cell growth and promotes apoptosis in retinoblastoma cells through regulating miR-99a and c-Myc

Wang

Zhang

Han

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

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Retinoblastoma is a rare cancer of the immature retina. This study designed to see the function of the lncRNA ANRIL in retinoblastoma Y79 cells. ANRIL, miR-99a and c-Myc expression in Y79 cells was altered by transfection and then trypan blue, transwell assay and flow cytometry were carried out to evaluate the changes of cell phenotype. The connection between ANRIL, miR-99a and c-Myc was measured by luciferase reporter assay and RNA immunoprecipitation analysis. As a result, ANRIL expression was highly expressed in human retinoblastoma tissue as relative to the adjacent noncancerous tissues. ANRIL suppression inhibited Y79 cells viability, migration, invasion, while promoted apoptosis. ANRIL negatively regulated miR-99a by binding to miR-99a. Silence of miR-99a reversed the ANRIL-knockdown effects on Y79 cells. miR-99a overexpression suppressed Y79 cell viability, migration, invasion, and enhanced apoptosis through downregulating c-Myc. Meanwhile, we found that miR-99a inhibited JAK/ STAT and PI3K/AKT pathways. To conclude, it seems that ANRIL suppression inhibits cell growth and metastasis in retinoblastoma Y79 cells by regulating miR-99a and c-Myc.

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Functional diversity of long non-coding RNAs in immune regulation

Cited by 66 publications

References 76 publications

Impaired lnc‐IL7R modulatory mechanism of Toll‐like receptors is associated with an exacerbator phenotype of chronic obstructive pulmonary disease

Impaired lnc‐IL7R modulatory mechanism of Toll‐like receptors is associated with an exacerbator phenotype of chronic obstructive pulmonary disease

LncRNA LINC00668 promotes cell proliferation, migration, invasion ability and EMT process in hepatocellular carcinoma by targeting miR-532-5p/YY1 axis

RETRACTED ARTICLE: Silence of lncRNA ANRIL represses cell growth and promotes apoptosis in retinoblastoma cells through regulating miR-99a and c-Myc

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