miR-181a negatively regulates NF-κB signaling and affects activated B-cell–like diffuse large B-cell lymphoma pathogenesis

Kozloski, Goldi A.; Jiang, Xiaoyu; Bhatt, Shruti; Ruiz, Jose W.; Vega, Francisco; Shaknovich, Rita; Melnick, Ari

doi:10.1182/blood-2015-11-680462

Cited by 44 publications

(36 citation statements)

References 54 publications

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“…In addition, miR-181a-5p was negatively modified by CRNDE, and the Wnt/b-catenin signaling regulated by it served as a powerful mediator underlying sepsis-correlated inflammation. 21,22 In addition, the activity of NF-jB could be undermined after stimulation of over-expressed miR-181a, 23 even though whether the inflammation-boosting capacity of NF-jB would be weakened by miR-181a remained uncertain. Furthermore, miR-181a-5p was additionally supposed as a modulator of immune responses in dendritic cells via negative modification of TNF-a.…”

Section: Introductionmentioning

confidence: 99%

Linkage of lncRNA CRNDE sponging miR-181a-5p with aggravated inflammation underlying sepsis

Wang

Yue

et al. 2019

Innate Immun

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This investigation was performed to verify whether lncRNA CRNDE sponging miR-181a-5p was involved with sepsisrelevant inflammatory dysfunctions. Aggregately 136 sepsis patients and 151 healthy people were recruited, and their fasting peripheral blood was gathered to detect expressions of CRNDE and miR-181a-5p. In addition, THP-1 cells were transfected with si-CRNDE, miR-181a-5p mimic, pcDNA3.1-TLR4 and si-TLR4, and then sepsis-specific inflammatory cytokines within the cells were quantified. The sponging relationships between CRNDE and miR-181a-5p, as well as between miR-181a-5p and TLR4, were ascertained by means of luciferase reporter gene assay. The experimental results revealed that over-expressed CRNDE and under-expressed miR-181a-5p were associated with shortened lifespan of sepsis patients. Mechanically, si-CRNDE-1 and miR-181a-5p mimic were able to reverse the promoting effects of LPS on production of NF-kB, TNF-a, IL-1b and IL-6 by THP-1 cells. Moreover, the expressional change of miR-181a-5p in THP-1 cells was in part owing to its being sponged by CRNDE. Lastly, TLR4, subjected to targeted modification of miR-181a-5p, was capable of disturbing the contribution of CRNDE and miR-181a-5p to THP-1 cells' release of NF-kB, TNF-a, IL-1b and IL-6. Collectively, the CRNDE/miR-181a-5p/TLR4 axis seemed to have potential in modifying sepsisrelated inflammatory pathogenesis, which offered a direction for sepsis diagnosis and treatment.

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Section: Introductionmentioning

confidence: 99%

Linkage of lncRNA CRNDE sponging miR-181a-5p with aggravated inflammation underlying sepsis

Wang

Yue

et al. 2019

Innate Immun

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“…Not only do miRNAs impact the transcriptome, they are now known to target and regulate proteins and DNA [17, 18]. Recent studies have started to implicate miRNAs in driving DLBCL progression [19–21], but which specific miRNA signatures impact DLBCL development or progression remains to be fully delineated. MicroRNAs have also been implicated with age.…”

Section: Introductionmentioning

confidence: 99%

A Circulating microRNA Signature Predicts Age-Based Development of Lymphoma

et al. 2017

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Extensive epidemiological data have demonstrated an exponential rise in the incidence of non-Hodgkin lymphoma (NHL) that is associated with increasing age. The molecular etiology of this remains largely unknown, which impacts the effectiveness of treatment for patients. We proposed that age-dependent circulating microRNA (miRNA) signatures in the host influence diffuse large B cell lymphoma (DLBCL) development. Our objective was to examine tumor development in an age-based DLBCL system using an inventive systems biology approach. We harnessed a novel murine model of spontaneous DLBCL initiation (Smurf2-deficient) at two age groups: 3 and 15 months old. All Smurf2-deficient mice develop visible DLBCL tumor starting at 15 months of age. Total miRNA was isolated from serum, bone marrow and spleen and were collected for all age groups for Smurf2-deficient mice and age-matched wild-type C57BL/6 mice. Using systems biology techniques, we identified a list of 10 circulating miRNAs being regulated in both the spleen and bone marrow that were present in DLBCL forming mice starting at 3 months of age that were not present in the control mice. Furthermore, this miRNA signature was found to occur circulating in the blood and it strongly impacted JUN and MYC oncogenic signaling. In addition, quantification of the miRNA signature was performed via Droplet Digital PCR technology. It was discovered that a key miRNA signature circulates throughout a host prior to the formation of a tumor starting at 3 months old, which becomes further modulated by age and yielded calculation of a ‘carcinogenic risk score’. This novel age-based circulating miRNA signature may potentially be leveraged as a DLBCL risk profile at a young age to predict future lymphoma development or disease progression as well as for potential innovative miRNA-based targeted therapeutic strategies in lymphoma.

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“…Mechanistically, miR-34a could target the 3′-UTR of Foxp1 [97]. In parallel, miR-181a, miR-146a, and miR-28 are revealed as tumor suppressor genes [98][99][100].…”

Section: B Cellsmentioning

confidence: 99%

Noncoding RNAs in cancer immunity: functions, regulatory mechanisms, and clinical application

Zhang

2020

Mol Cancer

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It is well acknowledged that immune system is deeply involved in cancer initiation and progression, and can exert both pro-tumorigenic and anti-tumorigenic effects, depending on specific microenvironment. With the better understanding of cancer-associated immune cells, especially T cells, immunotherapy was developed and applied in multiple cancers and exhibits remarkable efficacy. However, currently only a subset of patients have responses to immunotherapy, suggesting that a boarder view of cancer immunity is required. Non-coding RNAs (ncRNAs), mainly including microRNAs (miRNAs) and long noncoding RNAs (lncRNAs), are identified as critical regulators in both cancer cells and immune cells, thus show great potential to serve as new therapeutic targets to improve the response of immunotherapy. In this review, we summarize the functions and regulatory mechanisms of ncRNAs in cancer immunity, and highlight the potential of ncRNAs as novel targets for immunotherapy. Development of cancer immunology Cancer immunology was discovered by William Coley who speculated that a strep infection had reversed cancer growth in 1891 [10]. Over time, many studies have confirmed that homograft rejection could reject transplanted tumors [11-13]. Based on this viewpoint, in 1970 Macfarlane Burnet developed and systematically

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miR-181a negatively regulates NF-κB signaling and affects activated B-cell–like diffuse large B-cell lymphoma pathogenesis

Cited by 44 publications

References 54 publications

Linkage of lncRNA CRNDE sponging miR-181a-5p with aggravated inflammation underlying sepsis

Linkage of lncRNA CRNDE sponging miR-181a-5p with aggravated inflammation underlying sepsis

A Circulating microRNA Signature Predicts Age-Based Development of Lymphoma

Noncoding RNAs in cancer immunity: functions, regulatory mechanisms, and clinical application

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