MiR-93通过靶向SMAD5促进弥漫性大b细胞淋巴瘤的进展和化疗耐药。

IF 2.5 4区 医学 Q3 ENDOCRINOLOGY & METABOLISM
Xiang Fang, Qiang Huang, Li-Jun Dong, Qi-Huan Liu, Xiao-Na Miao, Jian Xiong, Xiao-Duan Jiang, Qiang Yu
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引用次数: 0

摘要

为了探讨miR-93在弥漫大b细胞淋巴瘤(DLBCL)细胞凋亡、迁移、侵袭和化疗耐药中的作用和机制,我们采用生物信息学和实时定量反转录PCR检测miR-93和SMAD5在DLBCL组织和细胞中的表达。在DLBCL样本中miR-93的表达明显上调。在DLBCL细胞(OCI-LY7和SU-DHL-8)中,miR-93通过增加抗凋亡蛋白Bcl-2的表达和降低cleaved caspase-3水平,增强了对长春新碱的化学耐药,抑制了细胞凋亡。此外,miR-93显著降低细胞凋亡率,促进细胞迁移和侵袭。总之,miR-93通过靶向和抑制SMAD5的表达,促进了恶性行为,增加了DLBCL细胞的化疗耐药。因此,抑制miR-93表达或提高SMAD5表达可能对DLBCL治疗至关重要。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
MiR-93 promotes the progression and chemoresistance of diffuse large B-cell lymphoma cells via targeting SMAD5.

ABSTARCTTo investigate the role and mechanism of miR-93 in apoptosis, migration, invasion and chemoresistance of diffuse large B-cell lymphoma (DLBCL) cells, bioinformatics and real-time quantitative reverse transcription PCR were employed to detect the expression of miR-93 and SMAD5 in DLBCL tissues and cells. There was a notable upregulation of miR-93 expression in DLBCL samples. In DLBCL cells (OCI-LY7 and SU-DHL-8), miR-93 enhanced the chemoresistance to vincristine and inhibited apoptosis by increasing the expression of the anti-apoptotic protein Bcl-2 and decreasing cleaved caspase-3 levels. Additionally, miR-93 significantly reduced apoptosis rates and promoted cell migration and invasion. Collectively, miR-93 promoted malignant behaviour and increased chemoresistance of DLBCL cells by targeting and inhibiting SMAD5 expression. Thus, inhibiting miR-93 expression or elevating SMAD5 expression is likely to be crucial for DLBCL treatment.

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来源期刊
Archives of Physiology and Biochemistry
Archives of Physiology and Biochemistry ENDOCRINOLOGY & METABOLISM-PHYSIOLOGY
CiteScore
6.90
自引率
3.30%
发文量
21
期刊介绍: Archives of Physiology and Biochemistry: The Journal of Metabolic Diseases is an international peer-reviewed journal which has been relaunched to meet the increasing demand for integrated publication on molecular, biochemical and cellular aspects of metabolic diseases, as well as clinical and therapeutic strategies for their treatment. It publishes full-length original articles, rapid papers, reviews and mini-reviews on selected topics. It is the overall goal of the journal to disseminate novel approaches to an improved understanding of major metabolic disorders. The scope encompasses all topics related to the molecular and cellular pathophysiology of metabolic diseases like obesity, type 2 diabetes and the metabolic syndrome, and their associated complications. Clinical studies are considered as an integral part of the Journal and should be related to one of the following topics: -Dysregulation of hormone receptors and signal transduction -Contribution of gene variants and gene regulatory processes -Impairment of intermediary metabolism at the cellular level -Secretion and metabolism of peptides and other factors that mediate cellular crosstalk -Therapeutic strategies for managing metabolic diseases Special issues dedicated to topics in the field will be published regularly.
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