Prognostic Value of MicroRNA-182 in Cancers: A Meta-Analysis

Wang, Fei; Zhong, Shanliang; Zhang, Haijun; Zhang, Wei; Zhang, Hongming; Wu, Xue; Chen, Baoan

doi:10.1155/2015/482146

Cited by 23 publications

(25 citation statements)

References 39 publications

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“…MiR-182-5p belongs to the miR-183 family and miR-182-5p is encoded on chromosome 7q31-34 [18]. Medimegh et al (2014) examined expression of miR-182 in the following three groups: TNBC, NTNBC (Non Triple Negative Breast Cancer; Luminal A, Luminal B and HER2 positive patients) and healthy controls.…”

Section: Discussionmentioning

confidence: 99%

Dysregulation of microRNAs in triple-negative breast cancer

et al. 2017

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Objectives: Triple-negative breast cancer (TNBC) is an aggressive subtype of breast cancer with limited treatment options and poor prognosis. TNBC is usually diagnosed at a relatively young age and is characterized by high risk of developing metastases. Some epigenetic regulation of gene expression is associated with TNBC. Expression of microRNAs (miRNAs) can serve as a potential tool for identifying critical biomarkers in TNBC.The aim of our study is to examine expression of selected miRNAs in TNBC and to assess the relationship between miRNA expression and clinicopathological factors. Material and methods:Expression levels of 19 selected miRNAs were compared between cancerous and normal breast tissues by use of qPCR method. We have evaluated the relationship between the expression level of miRNAs and clinicopathological factors such as: age, tumor size and lymph node status. Results:We found that in TNBC tissues, when compared with normal breast tissues, the expression of miR-190a, miR-136-5p and miR-126-5p was significantly reduced (p = 0.0041, p = 0.0007, p = 0.0007, respectively) whereas expression of miR-135b-5p and miR-182-5p was significantly increased (p = 0.0194, p = 0.0041, respectively). We found a linear trend for tumor size and expression of miR-126-5p (p = 0.0296) and miR-135b-5p (p = 0.0241). Conclusions:Our study confirms that miRNA expression profile is dysregulated in TNBC patients compared to healthy controls. and miR-182-5p may be associated with development and progression of TNBC.

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Section: Discussionmentioning

confidence: 99%

Dysregulation of microRNAs in triple-negative breast cancer

et al. 2017

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“…The amount of miR-182 is increased in breast tumors compared with normal breast tissue (39) and in serum of patients with breast cancer (40). High miR-182 is associated with worse outcome in a meta-analysis of 10 studies (41). Overexpression of miR-182 increases the sensitivity of breast cancer cell lines to poly(ADP-ribose) polymerase 1 (PARP1) inhibitors (28, 42), similar to that observed in BRCA1-deficient cells and tumors (42).…”

Section: Discussionmentioning

confidence: 99%

A TGFβ–miR-182–BRCA1 axis controls the mammary differentiation hierarchy

et al. 2016

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Maintenance of mammary functional capacity during cycles of proliferation and regression depend on appropriate cell fate decisions of mammary progenitor cells to populate an epithelium consisting of secretory luminal cells and contractile myoepithelial cells. It is well established that transforming growth factor β (TGFβ) restricts mammary epithelial cell proliferation and that sensitivity to TGFβ is decreased in breast cancer. Here we show that TGFβ also exerts control of mammary progenitor self-renewal and lineage commitment decisions by stringent regulation of breast cancer early onset 1 (BRCA1), which controls stem cell self-renewal and lineage commitment. Either genetic depletion of Tgfb1or transient blockade of TGFβ increased self-renewal of mammary progenitor cells in mice and cultured primary mammary epithelial cells, and also skewed lineage commitment towards the myoepithelial fate. TGFβ stabilized the expression of BRCA1 by suppressing miR-182. Ectopic expression of BRCA1 or antagonism of miR-182 in cultured TGFβ-deficient mammary epithelial cells restored lineage commitment. These findings reveal that TGFβ modulation of BRCA1 directs mammary epithelial cell fate and, since stem/progenitor cells are thought to be the cell of origin for aggressive breast cancer subtypes, suggest that TGFβdysregulation during carcinogenesis may promote distinct breast cancer subtypes.

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“…Longitudinal analysis of circulating miRNAs revealed rno‐miR‐182 as a potential predictive biomarker, which is 96% identical in sequence to its human homolog. miR‐182 is another oncomiR that is commonly upregulated in multiple cancers and predicts poor survival in patients . Chen et al observed that high levels of serum miR‐182 in patients with HCC were significantly associated with decreased survival after surgery.…”

Section: Discussionmentioning

confidence: 99%

Serum miR‐182 is a predictive biomarker for dichotomization of risk of hepatocellular carcinoma in rats

Livingstone

Johnson

Roebuck

et al. 2019

Molecular Carcinogenesis

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Exploration of animal models leads to discoveries that can reveal candidate biomarkers for translation to human populations. Herein, a model of hepatocarcinogenesis and protection was used in which rats treated with aflatoxin (AFB1) daily for 28 days (200 µg/kg BW) developed tumors compared with rats completely protected from tumors by concurrent administration of the chemoprotective agent, 1‐[2‐cyano‐3‐,12‐dioxooleana‐1,9(11)‐dien‐28‐oyl]imidazole (CDDO‐Im). Differential expression of miRNAs in tumors (AFB1) and nontumor (AFB1 + CDDO‐Im) bearing livers and their levels in sera over the life‐course of the animals was determined. miRNA transcriptome analysis identified 17 miRNAs significantly upregulated at greater than five‐fold in the tumors. The ten most dysregulated miRNAs judged by fold‐change and biological significance were selected for further study, including liver‐specific miR‐122‐5p. Validation of sequencing results by real‐time PCR confirmed the upregulation of the majority of these miRNAs in tumors, including miR‐182, as well as miR‐224‐5p as the most dysregulated of these miRNAs (over 400‐fold). The longitudinal analysis of levels of miR‐182 in sera demonstrated significant and persistent increases (5.13‐fold; 95% CI: 4.59‐5.70). The increase in miR‐182 was detected months before any clinical symptoms were present in the animals. By the terminal time point of the study, in addition to elevated levels of serum miR‐182, serum miR‐122‐5p was also found to be increased (>1.5‐fold) in animals that developed hepatocarcinomas. Thus, using the data from an unbiased discovery approach of the tissue findings, serum miR‐182 was found to track across the complex, multistage process of hepatocarcinogenesis opening an opportunity for translation to human populations.

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Prognostic Value of MicroRNA-182 in Cancers: A Meta-Analysis

Cited by 23 publications

References 39 publications

Dysregulation of microRNAs in triple-negative breast cancer

Dysregulation of microRNAs in triple-negative breast cancer

A TGFβ–miR-182–BRCA1 axis controls the mammary differentiation hierarchy

Serum miR‐182 is a predictive biomarker for dichotomization of risk of hepatocellular carcinoma in rats

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