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抗 miR-19a 在骨髓瘤细胞系中诱导对硼替佐米更好的反应性。

AntagomiR-19a Induced Better Responsiveness to Bortezomib in Myeloma Cell Lines.

作者信息

Kazemi Azam, Abroun Saeid, Soleimani Masoud

机构信息

Department of Haematology and Blood Banking, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, Iran.

Department of Haematology and Blood Banking, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, Iran. Email:

出版信息

Cell J. 2021 Oct;23(5):503-509. doi: 10.22074/cellj.2021.7302. Epub 2021 Aug 29.

DOI:10.22074/cellj.2021.7302
PMID:34837676
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8588822/
Abstract

OBJECTIVE

Multiple myeloma (MM) is the clonal proliferation of neoplastic plasma cells in the bone marrow. Although bortezomib (BTZ) is a crucial drug for the treatment of MM, drug resistance is a major problem. OncomiR-19a plays an oncogenic role in many cancers, including MM; however, the function of miR-19a in the pathogenesis of MM and drug resistance has not been completely identified. The present research aims to investigate the inhibition of miR-19a by an antagomir to determine BTZ responsiveness, and determine if miR-19a can be a prognostic biomarker for MM.

MATERIALS AND METHODS

In this experimental study, viability and apoptosis of myeloma cells were analysed by the colorimetric 3-(4, 5-Dimethylthiazol-2-yl)-2, 5-Diphenyltetrazolium Bromide (MTT) and Annexin V/propidium iodide (PI) flow cytometry assays. Quantitative real-time polymerase chain reaction (qRT-PCR) was implemented to evaluate the expression levels of miR-19a, its targets , B-cell lymphoma 2 (), and (antiapoptotic and cell cycle related genes) at the mRNA level.

RESULTS

miR-19a was downregulated and exacerbated in transfected cells treated with BTZ. The rate of apoptosis in the myeloma cells after BTZ treatment considerably increased, which indicated an increase in the mRNA of , and . A decrease in STAT3 was also observed.

CONCLUSION

OncomiR-19a, as a biomarker, may induce better responsiveness to BTZ in myeloma cell lines through its targets and . In the future, this biomarker may provide new therapeutic targets for MM.

摘要

目的

多发性骨髓瘤（MM）是骨髓中肿瘤性浆细胞的克隆性增殖。尽管硼替佐米（BTZ）是治疗MM的关键药物，但耐药性是一个主要问题。致癌miR-19a在包括MM在内的许多癌症中发挥致癌作用；然而，miR-19a在MM发病机制和耐药性中的作用尚未完全明确。本研究旨在研究抗miR-19a对miR-19a的抑制作用以确定BTZ反应性，并确定miR-19a是否可作为MM的预后生物标志物。

材料与方法

在本实验研究中，通过比色法3-（4,5-二甲基噻唑-2-基）-2,5-二苯基四氮唑溴盐（MTT）和膜联蛋白V/碘化丙啶（PI）流式细胞术分析骨髓瘤细胞的活力和凋亡情况。采用定量实时聚合酶链反应（qRT-PCR）在mRNA水平评估miR-19a及其靶标、B细胞淋巴瘤2（）、和（抗凋亡和细胞周期相关基因）的表达水平。

结果

在用BTZ处理的转染细胞中，miR-19a表达下调且加剧。BTZ处理后骨髓瘤细胞的凋亡率显著增加，这表明、和的mRNA增加。还观察到信号转导和转录激活因子3（STAT3）减少。

结论

致癌miR-19a作为一种生物标志物，可能通过其靶标和在骨髓瘤细胞系中诱导对BTZ更好的反应性。未来，这种生物标志物可能为MM提供新的治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7a9c/8588822/f5a05ddc0a94/Cell-J-23-503-g06.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7a9c/8588822/135bb15de86d/Cell-J-23-503-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7a9c/8588822/10c13cb9b983/Cell-J-23-503-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7a9c/8588822/5db1e23955cd/Cell-J-23-503-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7a9c/8588822/90dba41f692a/Cell-J-23-503-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7a9c/8588822/20a605c1a986/Cell-J-23-503-g05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7a9c/8588822/f5a05ddc0a94/Cell-J-23-503-g06.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7a9c/8588822/135bb15de86d/Cell-J-23-503-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7a9c/8588822/10c13cb9b983/Cell-J-23-503-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7a9c/8588822/5db1e23955cd/Cell-J-23-503-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7a9c/8588822/90dba41f692a/Cell-J-23-503-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7a9c/8588822/20a605c1a986/Cell-J-23-503-g05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7a9c/8588822/f5a05ddc0a94/Cell-J-23-503-g06.jpg

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