Down-regulated miR-148b increases resistance to CHOP in diffuse large B-cell lymphoma cells by rescuing Ezrin

Sun, Nana; Wang, Chenyi; Sun, Yiqun; Ruan, Yejiao; Huang, Yueyue; Su, Tong; Zhou, Xiaohai; Huang, He; Guo, Weidong; He, Min; Yao, Rongxin; Lin, Xiaoji

doi:10.1016/j.biopha.2018.06.093

Cited by 14 publications

(11 citation statements)

References 24 publications

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“…A similar result was seen in nasopharyngeal carcinoma as phosphorylated Ezrin expression was dependent on increased Rho kinase and protein kinase C activity (Tang et al, 2011). The oncogenic role of Ezrin is not limited to solid tumors as it has also been seen in blood cancers, such as diffuse large B-cell lymphoma, where the knockdown of Ezrin attenuated chemotherapy resistance (Pore et al, 2015;Sun et al, 2018).…”

Section: Ezrin and Other Cancersmentioning

confidence: 61%

Ezrin Mediates Invasion and Metastasis in Tumorigenesis: A Review

Song

Zhang

et al. 2020

Front. Cell Dev. Biol.

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Section: Ezrin and Other Cancersmentioning

confidence: 61%

Ezrin Mediates Invasion and Metastasis in Tumorigenesis: A Review

Song

Zhang

et al. 2020

Front. Cell Dev. Biol.

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“…And miR-10a suppresses cell proliferation and promotes cell apoptosis via targeting BCL6 in DLBCL [38]. The main reason for the poor results of DLBCL chemotherapy is that DLBCL cells are resistant to chemotherapeutic drugs [39]. It has been confirmed that miRNAs are closely associated with cancer chemosensitivity.…”

Section: Discussionmentioning

confidence: 98%

Clinical Features and Prognostic Impact of Coexpression Modules Constructed by WGCNA for Diffuse Large B-Cell Lymphoma

Xiao

Wang

Bai

2020

BioMed Research International

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Objective. Diffuse large B-cell lymphoma (DLBCL) is a highly aggressive malignant tumor, accounting for 30-40% of non-Hodgkin’s lymphoma. Our aim was to construct novel prognostic models of candidate genes based on clinical features. Methods. RNA-seq and clinical data of DLBCL were retrieved from TCGA database. Coexpression modules were constructed by WGCNA. Then, we investigated the interactions between modules and clinical features. By overall survival analysis, prognostic candidate genes from modules of interest were identified. A coexpression network of prognostic candidate genes was then constructed through WGCNA. GEPIA was used to analyze the expression of a candidate gene between DLBCL and normal samples. Results. 19 coexpression modules were constructed by 12813 genes from 52 DLBCL samples. The number of genes in modules ranged from 34 to 5457. We found that the purple module was significantly related with histological type (p value = 1e-04). Overall survival analysis revealed that MAFA-AS1, hsa-mir-338, and hsa-mir-891a were related with prognosis of DLBCL (p value = 0.027, 0.039, and 0.022, respectively). A coexpression network was constructed for the three prognostic genes. MAFA-AS1 was interacted with 36 genes, hsa-mir-891a was interacted with 11 genes, while no gene showed interaction with hsa-mir-338. Using GEPIA, we found that MAFA-AS1 showed low expression in DLBCL samples (p<0.01). Conclusion. We constructed a coexpression module related with histological type and identified three candidate genes (MAFA-AS1, hsa-mir-338, and hsa-mir-891a) that possessed potential value as prognostic biomarkers and therapeutic targets of DLBCL.

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“…Increased cell death was triggered by modulation of drug resistance through downregulation of the expression of MDR1 [41] or LMP1 [92] or by affecting PI3K/AKT survival pathways [87]. Moreover, human DLBCL xenografts in mouse models showed that overexpression of miR-148b sensitized tumors to CHOP, presumably via an Ezrin rescue-associated mechanism [93]. Together, these studies suggest the potential of miRNAs as chemosensitizers to enhance cancer therapy efficacy.…”

Section: Mirna Modulation Can Enhance Sensitivity To Other B Cell Neoplasia Treatmentsmentioning

confidence: 98%

miRNA-Based Therapies in B Cell Non-Hodgkin Lymphoma

Fuertes

Ramiro

Yébenes

2020

Trends in Immunology

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Non-Hodgkin lymphoma (NHL) is a diverse class of hematological cancers, many of which arise from germinal center (GC)-experienced B cells. Thus GCs, the sites of antibody affinity maturation triggered during immune responses, also provide an environment that facilitates B cell oncogenic transformation. miRNAs provide attractive and mechanistically different strategies to treat these malignancies based on their potential for simultaneous modulation of multiple targets. Here, we discuss the scientific rationale for miRNA-based therapeutics in B cell neoplasias and review recent advances that may help establish a basis for novel candidate miRNA-based therapies for B cell-NHL (B-NHL). miRNA-Based Therapies in B-NHLLymphomas arise from the neoplastic transformation of either T or B lymphocytes. About 95% of all human lymphomas originate in B cells, rather than T cells, and most of them (75-85%) arise from mature B cells that are germinal center (GC, see Glossary) experienced [1]. GCs are unique structures in which Ig genes are remodeled and are thus essential for the generation of high-affinity antibodies required for a proficient immune response. The production of highaffinity antibodies entails the introduction of mutations and DNA double-strand breaks in Ig genes and thus increases the risk of generating oncogenic events in mature B cells that transit through the GC [2,3]. Mature B cell neoplasia underlies the vast majority of lymphocyte-derived cancers, including most B-NHLs, such as diffuse large B cell lymphomas (DLBCLs), follicular lymphoma (FL), Burkitt lymphoma (BL), multiple myeloma (MM), and B cell chronic lymphocytic leukemia (CLL) [4]. It is estimated that B-NHL affects 1.3 million people worldwide [Global Cancer Observatory (GCO), World Health Organization i ].While some types of B-NHL progress relatively slowly and are considered indolent cancers, about 60% of them, including BL and DLBCL, are aggressive and require immediate intervention [1]. In general, the main treatments for mature B-NHL are chemotherapy, immunochemotherapy, and radiation therapy; however, a significant fraction of these cancers are refractory to these interventions or relapse after treatment [1,5]. There is therefore an urgent need for alternative therapeutic strategies to replace or complement current approaches. Advances in knowledge of the molecular mechanisms underlying lymphomagenesis have led to the design of promising new drugs that target specific genes and proteins involved in neoplasia development or maintenance. Clinically available strategies targeting B-NHL currently include: (i) immunotherapy with celldirected monoclonal antibodies and chimeric antigen receptor (CAR) T cell therapy; and (ii) signal transduction inhibitors, including proteasome inhibitors, histone deacetylase (HDAC) inhibitors, and B cell receptor (BCR) signaling kinase inhibitors [6]. The availability of targeted therapies has improved treatment options for certain B cell neoplasias in some patients. However, current targeted therapies have important ...

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Down-regulated miR-148b increases resistance to CHOP in diffuse large B-cell lymphoma cells by rescuing Ezrin

Cited by 14 publications

References 24 publications

Ezrin Mediates Invasion and Metastasis in Tumorigenesis: A Review

Ezrin Mediates Invasion and Metastasis in Tumorigenesis: A Review

Clinical Features and Prognostic Impact of Coexpression Modules Constructed by WGCNA for Diffuse Large B-Cell Lymphoma

miRNA-Based Therapies in B Cell Non-Hodgkin Lymphoma

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