miR‐191/DAB2 axis regulates the tumorigenicity of estrogen receptor‐positive breast cancer

Tian, Xinxin; Zhang, Baotong

doi:10.1002/iub.1705

Cited by 34 publications

(32 citation statements)

References 22 publications

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“…Our results showing lower DAB2 expression in EBV-positive GC cell lines than in EBV-negative cells support that DAB2 functions as a tumor suppressor in EBVaGC. That is consistent with previous reports showing DAB2 as a putative tumor suppressor in various cancer types [21][22][23][24][25][26][27][28][29][30][31]. Some EBV-negative GC cells which do not express miR-BART1-3p showed no or very little expression of DAB2.…”

Section: Discussionsupporting

confidence: 93%

“…Further, miR-191 promoted the cellular viability of estrogen receptor-positive breast cancer cells by directly suppressing the expression of DAB2 [25]. Additionally, the induction of DAB2 expression reduced cancer growth, migration, and invasion [21][22][23][24][25][27][28][29][30][31].…”

Section: Introductionmentioning

confidence: 99%

“…Disabled homolog 2 (DAB2) encodes a mitogen-responsive phosphoprotein that contains a phosphotyrosine-binding domain and a proline-rich domain involved in the regulation of clathrinmediated endocytosis as well as receptor-mediated signaling pathways [16][17][18][19][20]. DAB2 has been considered as a putative tumor suppressor in NPC [21,22] as well as ovarian [23,24], breast [25][26][27], prostate [28], and lung carcinoma [29,30]. Several human miRNAs have been reported to target DAB2, causing tumor promotion.…”

Section: Introductionmentioning

confidence: 99%

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Epstein-Barr virus miR-BART1-3p suppresses apoptosis and promotes migration of gastric carcinoma cells by targeting DAB2

2020

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Although Epstein-Barr virus (EBV) is known to encode over 40 different miRNAs of its own, the roles of most EBV miRNAs remain unknown. Disabled homolog 2 (DAB2) is a putative tumor suppressor, but its role in gastric carcinoma (GC), especially in EBV-associated GC, needs to be clarified. Our qRT-PCR and mRNA microarray results showed that DAB2 expression was down-regulated in EBV-positive GC cells compared to EBV-negative cells. Four BART miRNAs that might target DAB2 were predicted, and we found, using a luciferase reporter assay, that miR-BART1-3p directly targeted the 3'-UTR of DAB2. The miR-BART1-3p transfection decreased DAB2 expression at both mRNA and protein levels, while transfection of an inhibitor of miR-BART1-3p, miR-BART1-3p(i), increased DAB2 expression. In addition, miR-BART1-3p as well as siDAB2 increased migration and decreased apoptosis. Meanwhile, miR-BART1-3p(i) or pcDNA3.1-DAB2 transfection decreased migration and increased apoptosis in EBV-infected GC cells. Furthermore, decreased migration by miR-BART1-3p(i) was abrogated by co-transfected siDAB2, while decreased migration by miR-BART1-3p(i) was further suppressed by a co-transfected DAB2 over-expression vector. Our data suggest that miR-BART1-3p plays an important role in the tumorigenesis of EBV-associated GC by directly targeting DAB2.

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Section: Discussionsupporting

confidence: 93%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Epstein-Barr virus miR-BART1-3p suppresses apoptosis and promotes migration of gastric carcinoma cells by targeting DAB2

2020

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“…To investigate the clinical value of miR-383 in cholangiocarcinoma, levels of miR-383 expression were detected in 82 cholangiocarcinoma specimens that were divided into high expression of the miR-383 group (n = 41) and low expression of the miR-383 group (n = 41) based on the median value of miR-383 expression 15 Subsequently, we evaluated the relationship between miR-383 expression and clinical variables by the χ 2 test or the Fisher exact test. As shown in Table 2, we did not find a statistical correction between miR-383 expression and the patient's age, sex, HBV, and histological differentiation.…”

Section: The Expression Of Mir-383 Is Associated With Clinical Progmentioning

confidence: 99%

miR‐383 promotes cholangiocarcinoma cell proliferation, migration, and invasion through targeting IRF1

Wan

Chi

et al. 2018

J of Cellular Biochemistry

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Interferon regulatory factor 1 (IRF1) has been found to serve as a tumor suppressor in cholangiocarcinoma, and enabled prediction of clinical progression and prognosis in our previous study. The objective of the current study is to screen and identify valuable microRNAs (miR), which target IRF1 to regulate cholangiocarcinoma cell proliferation, migration, and invasion. High expression of miR-383 was observed in cholangiocarcinoma tissues and cells. Meanwhile, we found the predicted binding site of miR-383 on the IRF1 3'-untranslated region (3'-UTR) according to the miR target database. The miR-383 expression was negatively related to IRF1 messeneger RNA (mRNA) and protein expression in cholangiocarcinoma tissue samples, and miR-383 negatively regulated IRF1 mRNA and protein expression in cholangiocarcinoma cells. Subsequently, we conducted a luciferase reporter assay to prove the predicted binding site miR-383 on IRF1 3'-UTR. Moreover, the results of the rescue study suggested that IRF1 was a functional target of miR-383 involved in regulating cholangiocarcinoma cell proliferation, migration, and invasion. Finally, we evaluated the clinical and prognostic significance of miR-383 in cholangiocarcinoma cases, and found that high expression of miR-383 was correlated with advanced tumor stage, large tumor size, present vascular invasion, and metastasis, and acted as an unfavorable independent prognostic factor. In conclusion, miR-383 serves as a tumor-suppressive miR to regulate cholangiocarcinoma cell proliferation, migration, and invasion via directly targeting IRF1.

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“…17 DAB2 is a also a tumor suppressor gene and its expression is decreased in some tumors, such as breast cancer and nasopharyngeal carcinoma. 18,19 DAB2 has also been shown to negatively affect the function of various types of cells participating in the immune response. It is a target gene of forkhead box P3 (FOXP3), and DAB2-deficiency impairs the function of regulatory T cells.…”

mentioning

confidence: 99%

Disabled-2 (DAB2) Overexpression Inhibits Monocyte-Derived Dendritic Cells' Function in Vogt-Koyanagi-Harada Disease

Chang

et al. 2018

Invest. Ophthalmol. Vis. Sci.

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PURPOSE. Recent studies reported that the tumor suppressor disabled-2 (DAB2) is a negative regulator of immune function. In this study, we investigated the role of DAB2 in monocytederived dendritic cells (DCs) from Vogt-Koyanagi-Harada disease (VKH) patients. METHODS. The mRNA and protein levels of DAB2 were quantified by quantitative real-time PCR and Western blot. The Sequenom MassARRAY system was used to detect the promoter methylation level. An adenovirus carrying the DAB2 gene was transduced into immature DCs, isolated, and induced from active VKH patients. The surface markers of DCs, the frequency of T helper (Th) type 1 (Th1) and Th17 cells in CD4 þ T cells, which were cocultured with DCs, were tested by flow cytometry. ELISA was used to analyze the inflammatory cytokines produced by DC and CD4 þ T cell cocultures. RESULTS. The mRNA and protein expression levels of DAB2 in DCs obtained from active VKH patients were decreased, while the DAB2 promoter methylation level was marginally increased when compared with inactive VKH patients and normal controls. The expression of CD86 on DCs was significantly downregulated by DAB2 overexpression. The DC-related inflammatory factors IL-6 and TNF-a were also decreased. The frequency of Th1 and Th17 cells and their related cytokines were reduced significantly after coculture with DAB2 overexpressing DCs. DAB2 overexpression did not affect autophagy in DCs from VKH patients. CONCLUSIONS. These results suggest that the decreased expression of DAB2 in DCs plays a role in the pathogenesis of VKH disease. DAB2 overexpression inhibits DC function, but this is not mediated via autophagy.

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miR‐191/DAB2 axis regulates the tumorigenicity of estrogen receptor‐positive breast cancer

Cited by 34 publications

References 22 publications

Epstein-Barr virus miR-BART1-3p suppresses apoptosis and promotes migration of gastric carcinoma cells by targeting DAB2

Epstein-Barr virus miR-BART1-3p suppresses apoptosis and promotes migration of gastric carcinoma cells by targeting DAB2

miR‐383 promotes cholangiocarcinoma cell proliferation, migration, and invasion through targeting IRF1

Disabled-2 (DAB2) Overexpression Inhibits Monocyte-Derived Dendritic Cells' Function in Vogt-Koyanagi-Harada Disease

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