MicroRNA-451 suppresses tumor cell growth by down-regulating IL6R gene expression

Liu, Dong; Li, Cong; Wang, Xiyin; Ingvarsson, Sigurður; Chen, Huiping

doi:10.1016/j.canep.2013.12.005

Cited by 46 publications

(33 citation statements)

References 20 publications

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“…16 Furthermore, IL-6 also mediates the cross-talk between NF-kB and STAT-3 in human cancer cells. 33,34 In our study, we found that not only the production of IL-6 was decreased by GLA, but also the IL-6R signaling was blocked. In this study, we also found that GLA decreased the expression of IL-6R.…”

Section: Discussionsupporting

confidence: 50%

The repressive effect of miR-520a on NF-κB/IL-6/STAT-3 signal involved in the glabridin-induced anti-angiogenesis in human breast cancer cells

Ning

Wang

et al. 2015

RSC Adv.

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The formation of blood vessels plays a vital role in the growth of tumors. Breast cancer is a type of vascular dependent tumor, and angiogenesis plays an important role in its invasion and metastasis. Thus, the continued search for new mechanisms that inhibit the formation of blood vessels is becoming a strategy for the treatment of breast cancer. Glabridin (GLA) is a novel anti-tumor agent that inhibits oxidization, inflammation, and proliferation in human cancer cells. However, the functions of GLA in the regulation of angiogenesis in breast cancer and its underlying molecular mechanisms remain largely uninvestigated.In our present study, GLA attenuated the angiogenic ability by the microRNA-520a (miR-520a)-mediated inhibition of the NF-kB/IL-6/STAT-3 signal pathway in MDA-MB-231 and Hs-578T cells. Briefly, in these cells, GLA up-regulated the expression of miR-520a in a time-dependent manner; miR-520a, which targeted the NF-kB/RelA-3 0 UTR, decreased the expression/function of NF-kB, leading to the inactivation of IL-6/STAT-3 signaling; the knockdown of miR-520a abolished the GLA-induced inhibitions of the NF-kB/IL-6/STAT-3 signal pathway, the VEGF secretion, and the angiogenesis. By understanding the novel mechanism in which GLA inhibits the angiogenic potential in human breast cancer cells, our study would help in the design of future strategies in terms of developing GLA as a potential chemopreventive agent, when used alone or in combination with other current anticancer drugs.

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Section: Discussionsupporting

confidence: 50%

The repressive effect of miR-520a on NF-κB/IL-6/STAT-3 signal involved in the glabridin-induced anti-angiogenesis in human breast cancer cells

Ning

Wang

et al. 2015

RSC Adv.

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“…Analyses of the GO categories included several genes, which are relevant to cell proliferation, cell migration and invasion. As evidence has suggested that S100A6 regulates the levels of certain genes involved in cell proliferation, including IL-8 (24), IL-2 (25), IL-13 (26), IL-6R (27), CDK4 (28), CDK5 (29), MCM7 (30), Bcl2 (29) and MYC (31), these genes were selectively assessed. To confirm and to evaluate their expression levels, mRNA quantification was performed.…”

Section: Discussionmentioning

confidence: 99%

Increased expression of S100A6 promotes cell proliferation in gastric cancer cells

Wang

Lin

et al. 2016

Oncology Letters

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S100A6 is involved in regulating the progression of cancer. S100A6 can regulate the dynamics of cytoskeletal constituents, cell growth and differentiation by interacting with binding or target proteins. The present study investigated whether S100A6 affects cell proliferation in gastric cancer cells by stimulating several downstream factors. Firstly, the expression and localization of S100A6 were investigated using immunohistochemical staining, an immunoelectron microscopy and laser confocal scanning. A ChIP-Chip assay was performed to determine the downstream factors of S100A6 using promoter Chip analysis, including approximately the −800 to +200 regions around the transcription starting point. Polymerase chain reaction analysis was performed to confirm this. It was found that the intensity of S100A6 staining was markedly higher in the cytoplasm and nucleus, and its expression level correlated with that of the Ki67 protein. The overexpression of S100A6 also promoted cell proliferation in AGS and BGC823 cell lines, detected using a Cell Counting-Kit 8 assay. In cells overexpressing S100A6, the expression levels of interleukin (IL)-8, cyclin-dependent kinase (CDK)5, CDK4, minichromosome maintenance complex component 7 (MCM7) and B-cell lymphoma 2 (Bcl2) were noticeably increased. In conclusion, the increased expression of S100A6 promoted cell proliferation by regulating the expression levels of IL-8, CDK5, CDK4, MCM7 and Bcl2 in gastric cancer cells.

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“…Downregulation of miR‐451 increased the expression of its target gene, IL‐6R (an inflammatory cytokine) in both RKO and HeLa cells. It was discovered that miR‐451 has a tumor suppressor activity by targeting IL‐6R, so that its downregulation can induce inflammation, invasion, angiogenesis and proliferation in CC cells …”

Section: The Role and Function Of Micrornas In Cervical Cancer Inflammentioning

confidence: 99%

“…It was discovered that miR-451 has a tumor suppressor activity by targeting IL-6R, so that its downregulation can induce inflammation, invasion, angiogenesis and proliferation in CC cells. 112 Analysis of let-7 expression from malignant cervical tissues and in CaSki, SiHa and HeLa cell lines revealed that let-7 was markedly reduced during cervical carcinogenesis. Let-7a has been identified as a significant regulator of STAT3 levels.…”

Section: Hpv and Inflammation In Cervical Cancermentioning

confidence: 99%

Pathogenic role of exosomes and microRNAs in HPV‐mediated inflammation and cervical cancer: A review

Nahand

Moghoofei

Salmaninejad

et al. 2019

Intl Journal of Cancer

179

108

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Cervical cancer (CC) is the fourth most common cause of cancer death in women. The most important risk factor for the development of CC is cervical infection with human papilloma virus (HPV). Inflammation is a protective strategy that is triggered by the host against pathogens such as viral infections that acts rapidly to activate the innate immune response. Inflammation is beneficial if it is brief and well controlled; however, if the inflammation is excessive or it becomes of chronic duration, it can produce detrimental effects. HPV proteins are involved, both directly and indirectly, in the development of chronic inflammation, which is a causal factor in the development of CC. However, other factors may also have a potential role in stimulating chronic inflammation. MicroRNAs (miRNAs) (a class of noncoding RNAs) are strong regulators of gene expression. They have emerged as key players in several biological processes, including inflammatory pathways. Abnormal expression of miRNAs may be linked to the induction of inflammation that occurs in CC. Exosomes are a subset of extracellular vesicles shed by almost all types of cells, which can function as cargo transfer vehicles. Exosomes contain proteins and genetic material (including miRNAs) derived from their parent cells and can potentially affect recipient cells. Exosomes have recently been recognized to be involved in inflammatory processes and can also affect the immune response. In this review, we discuss the role of HPV proteins, miRNAs and exosomes in the inflammation associated with CC.

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MicroRNA-451 suppresses tumor cell growth by down-regulating IL6R gene expression

Cited by 46 publications

References 20 publications

The repressive effect of miR-520a on NF-κB/IL-6/STAT-3 signal involved in the glabridin-induced anti-angiogenesis in human breast cancer cells

The repressive effect of miR-520a on NF-κB/IL-6/STAT-3 signal involved in the glabridin-induced anti-angiogenesis in human breast cancer cells

Increased expression of S100A6 promotes cell proliferation in gastric cancer cells

Pathogenic role of exosomes and microRNAs in HPV‐mediated inflammation and cervical cancer: A review

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