miR-126 通过下调抗凋亡蛋白 MCL 诱导骨髓瘤细胞系 Karpas707 凋亡。

MiR-126 induces myeloma cell line Karpas707 apoptosis by downregulating anti-apoptotic protein MCL.

机构信息

Department of Orthopaedics, China-Japan Union Hospital of Jilin University, Changchun, China.

出版信息

Eur Rev Med Pharmacol Sci. 2018 Oct;22(20):6873-6879. doi: 10.26355/eurrev_201810_16156.

DOI:10.26355/eurrev_201810_16156

PMID:30402852

Abstract

OBJECTIVE

Myeloma seriously threats human life and health and needs more efficacy treatment method in the clinic. MiR-126 regulates cell proliferation and apoptosis. This study explores the regulatory role of miR-126 in myeloma and related molecular mechanism.

MATERIALS AND METHODS

MiR-126 and control were synthesized and transfected to myeloma cell line Karpas707 using Lipofectamine. Cell apoptosis was evaluated by MTT assay, caspase-3 activity detection, and flow cytometry. Myeloid cell leukemin (MCL) siRNA and plasmid were transfected to Karpas707 cells to test its impact on cell apoptosis.

RESULTS

MTT assay revealed that miR-126 significantly restrained Karpas707 cell growth (p=0.0017). Cell apoptosis detection showed that miR-126 significantly promoted phosphatidylserine eversion and caspase-3 activation (p=0.031), and downregulated MCL level (p=0.017). MCL siRNA markedly enhanced Karpas707 cell apoptosis induced by miR-126 (p=0.024), while the MCL overexpression apparently inhibited Karpas707 cell apoptosis induced by miR-126 (p=0.0073).

CONCLUSIONS

MiR-126 induces Karpas707 cell apoptosis by downregulating anti-apoptotic protein MCL, which provides a theoretical basis for the target selection of myeloma.

摘要

目的

骨髓瘤严重威胁人类生命健康，临床上需要更有效的治疗方法。miR-126 调节细胞增殖和凋亡。本研究探讨了 miR-126 在骨髓瘤中的调节作用及其相关分子机制。

材料与方法

采用脂质体将 miR-126 和对照物转染至骨髓瘤细胞系 Karpas707。通过 MTT 法、caspase-3 活性检测和流式细胞术评估细胞凋亡。转染髓样细胞白血病（MCL）siRNA 和质粒以检测其对细胞凋亡的影响。

结果

MTT 法显示 miR-126 显著抑制 Karpas707 细胞生长（p=0.0017）。细胞凋亡检测显示 miR-126 显著促进磷脂酰丝氨酸外翻和 caspase-3 活化（p=0.031），并下调 MCL 水平（p=0.017）。MCL siRNA 显著增强 miR-126 诱导的 Karpas707 细胞凋亡（p=0.024），而过表达 MCL 则明显抑制 miR-126 诱导的 Karpas707 细胞凋亡（p=0.0073）。