miR-130b, an onco-miRNA in bladder cancer, is directly regulated by NF-κB and sustains NF-κB activation by decreasing Cylindromatosis expression

Cui, Xiaolu; Kong, Chuize; Zhu, Yuyan; Zeng, Yu; Zhang, Zhe; Liu, Xiankui; Zhan, Bo; Piao, Chiyuan; Jiang, Zhenming

doi:10.18632/oncotarget.10423

Cited by 37 publications

(37 citation statements)

References 44 publications

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“…miRNAs 130b-3p, 27b, and 140, which were each elevated on our PCR array during sepsis, have all been shown to regulate inflammation, specifically via NF-jB [21][22][23]26]. After determining which inflammatory miRNAs had a propensity to become elevated in the blood during sepsis, we then reviewed the literature to decide which miRNAs to continue studying for their potential interaction with eCIRP.…”

Section: Discussionmentioning

confidence: 99%

Extracellular microRNA 130b‐3p inhibits eCIRP‐induced inflammation

et al. 2019

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Although microRNAs regulate mRNA expression intracellularly, they are often released into the circulation in inflammatory diseases. During sepsis, secreted extracellular cold-inducible RNAbinding protein (eCIRP) acts as a damage-associated molecular pattern (DAMP), inducing tissue damage by elevating inflammatory cytokines and chemokines. Here, we report that the circulating microRNA 130b-3p inhibits eCIRP-mediated sterile and cecal ligation and puncture (CLP)-induced non-sterile inflammation. We find that levels of miR-130b-3p are increased in the serum of septic mice and patients and that it strongly interacts with recombinant murine (rm) CIRP in vitro and with eCIRP in the serum of septic mice in vivo. Combining a miR-130b-3p mimic with rmCIRP significantly decreases TNF-a release by macrophages compared to only rmCIRP-treated cells. This combined treatment also dose-dependently decreases the affinity of rmCIRP with its receptor TLR4/ MD2. Finally, injection of a miR-130b-3p mimic significantly reduces rmCIRP-or CLP-induced systemic inflammation and acute lung injury in mice. These data show that extracellular miR-130b-3p functions as a novel endogenous inhibitor of eCIRP and point to an innovative therapeutic approach to treat inflammatory diseases.

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Section: Discussionmentioning

confidence: 99%

Extracellular microRNA 130b‐3p inhibits eCIRP‐induced inflammation

et al. 2019

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“…Although the roles of circRNAs remain a mystery, insights into circRNAs have revealed that several circRNAs can function as microRNA sponges (26). In addition, Cui et al (27) revealed that the nuclear factor-κ-B (NF-κB) signaling pathway could directly regulate transcription of miR-130b. Thus, the upstream regulation mechanism of miR-26-5p warrants further study.…”

Section: Discussionmentioning

confidence: 99%

miRNA‑26a‑5p and miR‑26b‑5p inhibit the proliferation of bladder cancer cells by regulating PDCD10

Jiang

et al. 2018

Oncol Rep

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MicroRNA (miR)-26a-5p and miR-26b-5p consistently play an antitumor role in many types of cancers, but the underlying mechanism remains unclear in bladder cancer (BC). In the present study, we found that, in BC tissues, the levels of miR-26a-5p and miR-26b-5p were lower than in paired normal tissues. The upregulation of miR-26-5p significantly inhibited the proliferation of BC cell lines (T24 and 5637). Bioinformatics analysis indicated that Programmed Cell Death 10 (PDCD10) was the downstream target gene of miR-26a-5p/miR-26b-5p, and this was ascertained by western blotting and quantitative real-time reverse transcription PCR (RT-qPCR). In addition, in the 3'-UTR of PDCD10, the binding site was identified using a luciferase reporter assay. We determined that clinical BC tissues presented higher PDCD10 levels than adjacent normal tissues and that PDCD10 promoted proliferation of BC cell lines. Overexpression of miR-26a-5p/miR-26b-5p inhibited the stimulatory effect on proliferation of BC cells induced by PDCD10. In addition, in vivo experiments and clinical data revealed that the prognosis of BC patients with high expression of miR-26a-5p/miR-26b-5p and low expression of PDCD10 was better than that of patients with low miR-26-5p and high PDCD10 expression. These data revealed that miR-26a-5p and miR-26b-5p were pivotal regulators in BC progression by targeting the proliferation-related protein, PDCD10. The miR-26-5p/PDCD10 interaction may provide important insight into the pathway of BC progression and present novel opportunities for future diagnosis and treatment strategies, especially for patients with high levels of PDCD10.

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“…The TNF‐α‐induced expressions of miR‐130b have been described in both adipocyte and bladder carcinoma cell lines . Through the analyses on the data from semiquantitative real‐time RT‐PCR assays, we found that the increment in the expression level of miR‐130b was in correlation with the elevation in the concentration of TNF‐α utilized to treat cell when the concentration of TNF‐α increased from 0 up to 10 ng·mL −1 .…”

Section: Resultsmentioning

confidence: 88%

“…A). The recent literatures illustrated that NF‐κB mediated the TNF‐α‐upregulated expressions of miR‐130b in both adipocyte and bladder carcinoma cell lines by directly binding to its response elements within the miR‐130b promoters . And it has been generally known that TNF‐α stimulation induced the activation of NF‐κB in Hela cell.…”

Section: Discussionmentioning

confidence: 99%

The TNF‐α‐induced expression of miR‐130b protects cervical cancer cells from the cytotoxicity of TNF‐α

et al. 2018

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Tumour necrosis factor alpha (TNF‐α) is a multifunctional cytokine and has the capacity both to promote cell growth and to kill tumour cells by inducing cell apoptosis. However, many tumour cells develop resistance to the toxic effects of TNF‐α. Thus, understanding the mechanism underlying the resistance of tumours to TNF‐α toxicity and finding ways to overcome this resistance are urgently needed. In this study, we discovered that two cervical cancer cell lines, Hela and Siha, showed null responses to TNF‐α cytotoxicity. However, in these cell lines, TNF‐α stimulation promoted the expression of miR‐130b and downregulated the expression of PTEN gene, which encodes a dual‐specificity phosphatase that acts as a tumour suppressor. Blockade of miR‐130b function or overexpression of PTEN gene sensitized cells to TNF‐α cytotoxicity. Regression analyses revealed that there were reverse relationships between the cellular levels of miR‐130b and PTEN mRNA in cervical cancer cells. Gain‐ and loss‐of‐function assays demonstrated that there were causal relationships between the increase in miR‐130b levels and the reduction in PTEN mRNA or PTEN protein levels. In silico analysis revealed that there were two miR‐130b target sites within the 3′UTR of PTEN mRNA and experimental evidences demonstrated that miR‐130b repressed the expression of PTEN gene by binding directly to the 3′UTR of PTEN mRNA. These data suggest miR‐130b expression as a target to be inhibited to make tumour cells more sensitive to the toxic impact of TNF‐α.

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miR-130b, an onco-miRNA in bladder cancer, is directly regulated by NF-κB and sustains NF-κB activation by decreasing Cylindromatosis expression

Cited by 37 publications

References 44 publications

Extracellular microRNA 130b‐3p inhibits eCIRP‐induced inflammation

Extracellular microRNA 130b‐3p inhibits eCIRP‐induced inflammation

miRNA‑26a‑5p and miR‑26b‑5p inhibit the proliferation of bladder cancer cells by regulating PDCD10

The TNF‐α‐induced expression of miR‐130b protects cervical cancer cells from the cytotoxicity of TNF‐α

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