LncRNA MALAT1沉默可通过抑制CXCR4抑制CXCL12诱导的多发性骨髓瘤的增殖、侵袭和归巢行为。

IF 2 4区 医学 Q3 HEMATOLOGY
Hematology Pub Date : 2024-12-01 Epub Date: 2024-11-06 DOI:10.1080/16078454.2024.2422154
Jing Ning, Rui Yang, Hainan Wang, Hui Ma, Lijuan Cui
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引用次数: 0

摘要

背景:在多发性骨髓瘤(MM)中发现了长非编码RNA转移相关肺腺癌转录本1(MALAT1),但其对MM细胞归巢行为的影响尚不清楚。本研究阐明了MALAT1对MM细胞归巢行为的影响及其机制:方法:从 MM 患者身上获取骨髓。通过 qRT-PCR 和 Western 印迹法检测分化簇 138 纯化(CD138)浆细胞中 MALAT1 和 C-X-C motif 趋化因子受体 4(CXCR4)的表达。通过CCK-8、5-乙炔基-2'-脱氧尿苷和Transwell试验监测了MALAT1、CXCR4和C-X-C位点趋化因子配体12(CXCL12)对MM细胞活力、增殖和侵袭的影响;利用qRT-PCR、Western印迹和ELISA检测了MM细胞中与归巢效应相关的蛋白,包括细胞间粘附分子1(ICAM-1)和晚期抗原-4(VLA-4):结果:MM 患者骨髓中 CD138 纯化的浆细胞中 MALAT1 和 CXCR4 过表达,这与骨损伤有关。MALAT1能上调MM细胞中的CXCR4。MALAT1 的过表达增强了 MM 细胞的活力、增殖和侵袭,而 CXCR4 的沉默则逆转了它们。沉默 CXCR4 可减轻 MALAT1 对 MM 细胞中 ICAM-1 和 VLA-4 表达的诱导。CXCL12 的上调增强了 MM 细胞的增殖和侵袭以及 ICAM-1 和 VLA-4 的表达。沉默MALAT1可抵消CXCL12的影响:结论:沉默 MALAT1 可通过抑制 CXCR4 抑制 CXCL12 对 MM 细胞增殖、侵袭和归巢行为的诱导。结论:MALAT1沉默可通过抑制CXCR4抑制CXCL12对MM细胞增殖、侵袭和归巢行为的诱导。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
LncRNA MALAT1 silencing represses CXCL12-induced proliferation, invasion, and homing behavior in multiple myeloma by inhibiting CXCR4.

Background: Long non-coding RNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) has been identified in multiple myeloma (MM); its influence on the homing behavior in MM cells is unclear. This study elucidates the impact and mechanism by which MALAT1 affects the homing behavior in MM cells.

Methods: Bone marrow was obtained from patients with MM. MALAT1 and C-X-C motif chemokine receptor 4 (CXCR4) expression in cluster of differentiation 138-purified (CD138) plasma cells were detected by qRT-PCR and Western blotting. MALAT1, CXCR4, and C-X-C motif chemokine ligand 12 (CXCL12) influences on MM cell viability, proliferation, and invasion was monitored by CCK-8, 5-Ethynyl-2'-deoxyuridine, and Transwell assays. qRT-PCR, Western blotting, and ELISA were utilized to detect homing effect-related proteins in MM cells, including intercellular adhesion molecule 1 (ICAM-1) and very late antigen-4 (VLA-4).

Results: MALAT1 and CXCR4 were overexpressed in CD138-purified plasma cells from bone marrow of MM patients, associating with bone damage. MALAT1 upregulated CXCR4 in MM cells. MALAT1 overexpression enhanced MM cell viability, proliferation, and invasion, whereas CXCR4 silencing reversed them. CXCR4 silencing attenuated MALAT1 induction on ICAM-1 and VLA-4 expression in MM cells. CXCL12 upregulation intensified MM cell proliferation and invasion and ICAM-1 and VLA-4 expression in MM cells. MALAT1 silencing counteracted the impact of CXCL12.

Conclusion: MALAT1 silencing may repress CXCL12 induction on MM cell proliferation, invasion, and homing behavior by inhibiting CXCR4. MALAT1 may be a promising target for MM treatment.

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来源期刊
Hematology
Hematology 医学-血液学
CiteScore
2.60
自引率
5.30%
发文量
140
审稿时长
3 months
期刊介绍: Hematology is an international journal publishing original and review articles in the field of general hematology, including oncology, pathology, biology, clinical research and epidemiology. Of the fixed sections, annotations are accepted on any general or scientific field: technical annotations covering current laboratory practice in general hematology, blood transfusion and clinical trials, and current clinical practice reviews the consensus driven areas of care and management.
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