MicroRNA-21 and the clinical outcomes of various carcinomas: a systematic review and meta-analysis

Wang, Wenjia; Li, Jinhui; Zhu, Wei; Gao, Chen; Jiang, Ruijingfang; Li, Wenxue; Hu, Qiansheng; Zhang, Bo

doi:10.1186/1471-2407-14-819

Cited by 65 publications

(38 citation statements)

References 64 publications

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“…miR-21 has been reported to be one of the most commonly up-regulated miRNAs in various human cancers functioning as a key regulator of carcinogenic process, and has been considered as a novel target in cancer therapeutics (Selcuklu et al, 2009; Krichevsky and Gabriely, 2009; Pan et al, 2010; Kumarswamy et al, 2011; Wang et al, 2014a). It is interesting that recent studies also show that miR-21 is critically involved in arsenic-induced cell malignant transformation and tumorigenesis.…”

Section: The Role Of Mirnas In Metal Carcinogen-induced Cell Maligmentioning

confidence: 99%

The role of microRNAs in metal carcinogen-induced cell malignant transformation and tumorigenesis

Humphries

Wang

Yang

2016

Food and Chemical Toxicology

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MicroRNAs (miRNAs), an important component of epigenetic mechanisms of carcinogenesis, have been shown to play crucial roles in cancer initiation, metastasis, prognosis and responses to drug treatment and may serve as biomarkers for early diagnosis of cancer and tools for cancer therapy. Metal carcinogens, such as arsenic, cadmium, hexavalent chromium and nickel, are well-established human carcinogens causing various cancers upon long term exposure. However, the mechanism of metal carcinogenesis has not been well understood, which limits our capability to effectively diagnose and treat human cancers resulting from chronic metal carcinogen exposure. Over recent years, the role of miRNAs in metal carcinogenesis has been actively explored and a growing body of evidence indicates the critical involvement of miRNAs in metal carcinogenesis. This review aims to discuss recent studies showing that miRNAs play important roles in metal carcinogen-induced cell malignant transformation and tumorigenesis. Some thoughts for future further studies in this field are also presented.

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Section: The Role Of Mirnas In Metal Carcinogen-induced Cell Maligmentioning

confidence: 99%

The role of microRNAs in metal carcinogen-induced cell malignant transformation and tumorigenesis

Humphries

Wang

Yang

2016

Food and Chemical Toxicology

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“…The axis FASLG/miR-21 may also represent an important molecular mechanism in ALPS-FAS pathophysiology, as soluble FASLG is augmented in patients [19]. Moreover, growing evidence from recent studies has shown the involvement of miR-21 in several cancers [20]. Its upregulation, particularly in cancerous tissue, is effectively predictive of worse prognosis in multiple carcinomas [21].…”

Section: T Cell Receptor (Tcr)abmentioning

confidence: 99%

“…The role of miR-21 in several types of cancers is well documented [20]. Due to the apoptotic defect, ALPS patients are prone to develop lymphoma [2].…”

Section: Microrna-21-3p Up-regulation In Alps-fasmentioning

confidence: 99%

Differential regulation of miR-146a/FAS and miR-21/FASLG axes in autoimmune lymphoproliferative syndrome due to FAS mutation (ALPS-FAS)

Marega

Teocchi

Vilela

2016

Clinical and Experimental Immunology

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1These authors contributed equally to the study. SummaryMost cases of autoimmune lymphoproliferative syndrome (ALPS) have an inherited genetic defect involving apoptosis-related genes of the FAS pathway. MicroRNAs (miRNAs) are a class of small non-coding regulatory RNAs playing a role in the control of gene expression. This is the first report on miRNAs in ALPS patients. We studied a mother and son carrying the same FAS cell surface death receptor (FAS) mutation, but with only the son manifesting the signs and symptoms of ALPS-FAS. The aim was to analyse, by reverse transcription-quantitative polymerase chain reaction (RT-qPCR), the peripheral blood mononuclear cells (PBMC) relative expression of miR-146a and miR-21, including their passenger strands and respective targets (FAS and FASLG). In comparison with healthy matched control individuals, miR-21-3p was over-expressed significantly (P 5 0Á0313) in the son, with no significant change in the expression of miR-146a, miR-146a-3p and miR-21. In contrast, the mother had a slight under-expression of the miR-146a pair and miR-21-3p (P 5 0Á0625). Regarding the miRNA targets, FAS was up-regulated markedly for the mother (P 5 0Á0078), but down-regulated for the son (P 5 0Á0625), while FASLG did not have any significant alteration. Taken together, our finding clearly suggests a role of the miR-146a/FAS axis in ALPS-FAS variable expressivity in which FAS haploinsufficiency seems to be compensated only in the mother who had the miR-146a pair down-regulated. As only the son had the major clinical manifestations of ALPS-FAS, miR-21-3p should be investigated as playing a critical role in ALPS physiopathology, including the development of lymphoma.

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“…MiR-21 was described as an oncomiR and implicated in tumor progression of various cancers [12–15]. Of interest, up-regulation of miR-21 was associated with lung cancer diagnosis and prognosis, indicating a potential role of miR-21 in human lung cancer progression [16, 17].…”

Section: Introductionmentioning

confidence: 99%

TLR4/ROS/miRNA-21 pathway underlies lipopolysaccharide instructed primary tumor outgrowth in lung cancer patients

et al. 2016

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Activation of Toll-like receptor 4 (TLR4) signaling in human lung cancer with lipopolysaccharide (LPS) enhances tumor progression. However, whether primary human lung cancer outgrowth could respond to LPS and underlying mechanisms are unclear. Here we determined that TLR4 activation with LPS promoted outgrowth of primary human lung cancer cells in vitro and in vivo. Mechanistically, LPS stimulation increased expression levels of microRNA-21 (miR-21) in primary human lung cancer cells. Inhibition of miR-21 blocked the enhanced lung cancer growth induced by LPS in vitro and in vivo. Up-regulation of miR-21 promoted outgrowth of primary human lung cancer. Down-regulation of miR-21 limited primary human lung cancer outgrowth. Further, TLR4 activation in primary human lung cancer cells increased their ROS levels. Scavenge of ROS abrogated the up-regulation of miR-21 in primary human lung cancer cells and attenuated LPS-induced outgrowth. For in vivo relevance, expression of TLR4 was correlated with miR-21 expression and ROS production in freshly isolated, untreated primary human lung cancer cells. These findings demonstrate an essential role of TLR4/ROS/miR-21 pathway in LPS-induced outgrowth of primary human lung cancer. Our study connected a framework of innate signaling, oxidative stress and microRNA in tumor immunity and provided clues for developing new therapeutics for lung cancer.

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MicroRNA-21 and the clinical outcomes of various carcinomas: a systematic review and meta-analysis

Cited by 65 publications

References 64 publications

The role of microRNAs in metal carcinogen-induced cell malignant transformation and tumorigenesis

The role of microRNAs in metal carcinogen-induced cell malignant transformation and tumorigenesis

Differential regulation of miR-146a/FAS and miR-21/FASLG axes in autoimmune lymphoproliferative syndrome due to FAS mutation (ALPS-FAS)

TLR4/ROS/miRNA-21 pathway underlies lipopolysaccharide instructed primary tumor outgrowth in lung cancer patients

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