Abstract
miRNAs are non-coding RNA molecules; their deregulations may contribute to cancer pathogenesis. However, the mechanisms of how miRNA dysfunction contributes to the lymphomagenesis of diffuse large B-cell lymphoma (DLBCL) are not well established. In this study, we analyzed the expression of miR-224 in four DLBCL cell lines and 168 patients’ specimens. We found that the expression of miR-224 in DLBCL was down-regulated compared with normal B-cell but was not statistically different between the germinal center B-cell-like-type and the activated B-cell-like-type. Using bioinformatics prediction and luciferase report assays, we demonstrated that miR-224 directly down-regulated CD59 expression by binding to its 3’-untranslated region. We also used immunohistochemical staining of CD59 in human DLBCL specimens and analyzed the relationship between the expression of miR-224, CD59 and the overall/progress-free survival of DLBCL patients who were uniformly treated with rituximab,cyclophosphamide, adriamycin, vincristine, and prednisone (R-CHOP). We found that miR-224 may contribute to DLBCL pathogenesis. Most importantly, the expression of miR-224 and CD59 can predict the response and outcome of DLBCL patients treated with R-CHOP.
Keywords: CD59, diffuse large B-cell lymphoma (DLBCL), microRNA (miRNA), miR-224, R-CHOP.
Current Cancer Drug Targets
Title:Deregulated Expression of miR-224 and its Target Gene: CD59 Predicts Outcome of Diffuse Large B-cell Lymphoma Patients Treated with R-CHOP
Volume: 14 Issue: 7
Author(s): Guoqi Song, Guorong Song, Huiyun Ni, Ling Gu, Hong Liu, Baoan Chen, Bangshun He, Yuqin Pan, Shukui Wang and William C. Cho
Affiliation:
Keywords: CD59, diffuse large B-cell lymphoma (DLBCL), microRNA (miRNA), miR-224, R-CHOP.
Abstract: miRNAs are non-coding RNA molecules; their deregulations may contribute to cancer pathogenesis. However, the mechanisms of how miRNA dysfunction contributes to the lymphomagenesis of diffuse large B-cell lymphoma (DLBCL) are not well established. In this study, we analyzed the expression of miR-224 in four DLBCL cell lines and 168 patients’ specimens. We found that the expression of miR-224 in DLBCL was down-regulated compared with normal B-cell but was not statistically different between the germinal center B-cell-like-type and the activated B-cell-like-type. Using bioinformatics prediction and luciferase report assays, we demonstrated that miR-224 directly down-regulated CD59 expression by binding to its 3’-untranslated region. We also used immunohistochemical staining of CD59 in human DLBCL specimens and analyzed the relationship between the expression of miR-224, CD59 and the overall/progress-free survival of DLBCL patients who were uniformly treated with rituximab,cyclophosphamide, adriamycin, vincristine, and prednisone (R-CHOP). We found that miR-224 may contribute to DLBCL pathogenesis. Most importantly, the expression of miR-224 and CD59 can predict the response and outcome of DLBCL patients treated with R-CHOP.
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Song Guoqi, Song Guorong, Ni Huiyun, Gu Ling, Liu Hong, Chen Baoan, He Bangshun, Pan Yuqin, Wang Shukui and Cho C. William, Deregulated Expression of miR-224 and its Target Gene: CD59 Predicts Outcome of Diffuse Large B-cell Lymphoma Patients Treated with R-CHOP, Current Cancer Drug Targets 2014; 14 (7) . https://dx.doi.org/10.2174/1568009614666140818211103
DOI https://dx.doi.org/10.2174/1568009614666140818211103 |
Print ISSN 1568-0096 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-5576 |
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