BRG1 regulation by miR-155 in human leukemia and lymphoma cell lines

Cuadros, Marta; Sánchez-Martín, Victoria; Herrera, Antonio Mateos; Baliñas, Carlos; Martín-Padrón, Joel; Boyero, Laura; Peinado, Paola; Medina, Pedro P.

doi:10.1007/s12094-017-1633-2

Cited by 12 publications

(10 citation statements)

References 29 publications

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“…miR-155 directly inhibited the expression of BRG1 and upregulated the subsequent VEGFC, but not VEGFD expression in NKTCLs miR-155 negatively regulated BRG1 expression in human leukemia cell lines. 30 To assess whether miR-155 directly inhibited BRG1 transcription, we cloned the 3-UTR sequence of BRG1 that contained the potential miR-155 binding site (WT) or a mutated sequence (MUT) into a luciferase reporter construct. As shown in Figure 2(a), miR-155 potently inhibited the luciferase activity from the WT but not from the MUT construct, suggesting that miR-155 can directly and specifically inhibit the transcription of BRG1.…”

Section: Discussionmentioning

confidence: 99%

“…In addition to NKTCL cells, Cuadros et al reported the negative correlation between miR-155 and BRG1 in different lymphoma cells. 30 As either a tumor suppressor or an oncogene, BRG1 presented pleotropic phenotypes mostly through the association and expressional regulation of different target genes, such as: RB family proteins, [43][44][45] p21, 46 and p53, 47 for viability and cell cycle progression; p53, 47 BRCA1, 48 and FANCA 49 for DNA repair; CD44 50 and E-cadherin for cell adhesion; multiple genes in T-cell development and other immune functions 51 ; miR-550a-5p/RNF43/Wnt/β-catenin signaling 28 and miR-148b 52 for cancer metastasis. Recently, Zhu et al showed that by inhibiting the activation of STAT3 and subsequently the expression of VEGFC, BRG1 controlled lymphangiogenesis in colorectal carcinoma, both in vitro and in vivo.…”

Section: Discussionmentioning

confidence: 99%

“…29 In human leukemia and lymphoma cell lines, miR-155 suppressed the expression of BRG1. 30 However, the status of BRG1 in NKTCL is not well characterized, nor is the potential roles and mechanisms of miR-155/BRG1 signaling in the progression of NKTCL.…”

Section: Introductionmentioning

confidence: 99%

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MiRNA-155 regulates lymphangiogenesis in natural killer/T-cell lymphoma by targeting BRG1

Chang

Cui

et al. 2018

Cancer Biology & Therapy

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Background: miR-155 was up-regulated in natural killer/T-cell lymphoma (NKTCL), an aggressive malignancy, and correlated with disease progression. However, minimal is known on biological activities and underlying mechanisms of miR-155 in NKTCL. In this study, we examined BRG1, a potential target of miR-155, and focused on the miR-155/BRG1 signaling in regulating lymphangiogenesis of NKTCL. Methods: The expression of miR-155, BRG1, VEGFC, and VEGFD was compared between two NKTCL cell lines and normal NK cells. The critical role of miR-155 and STAT3 was assessed using miR-155 inhibitor and STAT3 inhibitor S31-201, respectively. Two biological phenotypes, apoptosis and pro-lymphangiogenesis, were examined in vitro by flow cytometry and lymphatic tube formation, respectively, and in vivo using an NKTCL xenograft model. Results: The miR-155 level negatively correlated with BRG1, but positively with VEGFC in normal NK as well as two NKTCL cell lines. Targeting miR-155 in NKTCL cells significantly boosted BRG1 expression and decreased the activated STAT3 or VEGFC level, leading to enhanced apoptosis and reduced lymphangiogenesis. STAT3 acted downstream of BRG1 and essentially regulated miR-155-mediated up-regulation of VEGFC and pro-lymphangiogenesis. In vivo, targeting miR-155 inhibited primary xenograft growth as well as tumor-associated lymphangiogenesis. Conclusions: By inhibiting BRG1 expression, miR-155 activated STAT3/VEGFC signaling and promoted lymphangiogenesis. In addition, miR-155 also controlled the viability of NKTCL cells. Therefore, targeting miR-155 provides a novel therapy for NKTCL.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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MiRNA-155 regulates lymphangiogenesis in natural killer/T-cell lymphoma by targeting BRG1

Chang

Cui

et al. 2018

Cancer Biology & Therapy

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“…In their previous study, it was found that a lack of BRG1 in lung tumors could be related to the action of different miRNAs, such as miR-155. The authors, in 2018, found that BRG1 levels were inversely proportional to miR-155 expression in Burkitt’s lymphoma and the diffuse large B cell lymphoma human cell line [ 27 ]. Chang et al, in 2019, reported that miR-155 regulates lymphangiogenesis in NKTCL through the miR-155/BRG1/STAT3/VEGFC pathways in human NKTCL cell lines.…”

Section: Resultsmentioning

confidence: 99%

Involvement of miR-142 and miR-155 in Non-Infectious Complications of CVID

et al. 2020

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Background and objectives: Common variable immunodeficiency (CVID) is the most prevalent antibody impairment. It is characterized by failure in immunoglobulin and protective antibody generation and defined by an increased tendency toward bacterial infections, autoimmunity, and malignancy. Most CVID diagnoses do not follow a classical Mendelian pattern of inheritance. In recent years, CVID has been considered an epigenetic phenomenon in the majority of cases, overtaking previous monogenetic and/or polygenetic theories. The aim of this study was to review the role of microRNAs (miRNAs) in CVID, focusing on the involvement of the same miRNAs in various non-infectious clinical complications of CVID, mainly autoimmunity and/or cancer. Materials and Methods: A bibliographic search of the scientific literature was carried out independently by two researchers in scientific databases and search engines. The MeSH terms “microRNAs” and “common variable immunodeficiency” were used. All research articles from inception to May 2020 were considered. Results: The literature data showed the involvement of two miRNAs in primary immunodeficiency: miR-142 and miR-155. Both of these miRNAs have been investigated through mice models, in which miR-142 and miR-155 were deleted. These knock-out (KO) mice models showed phenotypic analogies to CVID patients with hypogammaglobulinemia, adaptive immunodeficiency, polyclonal proliferation, lung disease, and enteric inflammation. miR-142 and miR-155 have been found to be involved in the following autoimmune and neoplastic clinical complications of CVID: Gastric cancer, gastric mucosa-associated lymphoid tissue (MALT) lymphoma, natural killer/Tcell lymphoma (NKTCL), and immune thrombocytopenia. Conclusions: miR-142 and miR-155 deregulation leads to similar CVID phenotypesin KO mice models. Although no data are available on the involvement of these miRNAs in human CVID, their dysregulation has been detected in human CVID comorbidities. The literature data show that miRNA sequences in murine models are comparable to those in humans; therefore, miR-142 and miR-155 involvement in human CVID could be hypothesized.

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“…These findings managed to link inflammation to cell transformation during cancer [ 124 ]. miR-155 has been also identified to exhibit antiapoptotic effects, overexpressed in inflammatory conditions [ 125 ] and leukemia [ 126 ], and which is responsible for the repression of proapoptotic tumor p53-induced nuclear protein 1 [ 127 ]. On the other hand, overexpression of miR-146b alters the NF- κ B signaling pathway in an IL-6-dependent manner, leading to a decrease in the invasion rate of breast cancer cells [ 128 ].…”

Section: Molecular Inflammatory Events During Cancer Development Amentioning

confidence: 99%

Inflammation and Inflammasomes: Pros and Cons in Tumorigenesis

Balahura

Șelaru

Dinescu

et al. 2020

Journal of Immunology Research

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Over the past decade, it has been well established that tumorigenesis is affected by chronic inflammation. During this event, proinflammatory cytokines are produced by numerous types of cells, such as fibroblasts, endothelial cells, macrophages, and tumor cells, and are able to promote the initiation, progression, and metastasis of different types of cancer. When persistent inflammation occurs, activation of inflammasome complexes is initiated, leading to its assembly and further activation of caspase, production of proinflammatory cytokines, and pyroptosis induction. The function of this multiprotein complex is not only to reassure inflammation and to promote cell death, through caspase activity, but also has been identified to have significant contributions during tumorigenesis and cancer development. So far, many efforts have been made in order to extend the knowledge of inflammasome implications and how its components could be targeted as therapeutic agents. Additionally, microRNAs (miRNAs), evolutionary conserved noncoding molecules, have emerged as pivotal players during numerous biological events by regulating gene and protein expression. Therefore, dysregulations of miRNA expressions have been correlated with inflammation during tumor development. In this review, we aim to highlight the dual role of inflammasomes and proinflammatory cytokines during carcinogenesis paired with the distinguished effects of miRNAs upon inflammation cascades during tumor growth and progression.

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BRG1 regulation by miR-155 in human leukemia and lymphoma cell lines

Cited by 12 publications

References 29 publications

MiRNA-155 regulates lymphangiogenesis in natural killer/T-cell lymphoma by targeting BRG1

MiRNA-155 regulates lymphangiogenesis in natural killer/T-cell lymphoma by targeting BRG1

Involvement of miR-142 and miR-155 in Non-Infectious Complications of CVID

Inflammation and Inflammasomes: Pros and Cons in Tumorigenesis

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