METTL3/MALAT1轴在多发性骨髓瘤进展中的调节作用

IF 3.4 2区医学 Q2 Medicine

Journal of Bone Oncology Pub Date : 2025-06-12 DOI:10.1016/j.jbo.2025.100695

Xiaohong Lu, Yafei Li, Ruie Li, Jingheng Zhang, Jiayu Peng, Yan Zhang

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引用次数: 0

摘要

目的甲基转移酶样3 （METTL3）在m6A修饰依赖性和非依赖性途径中都在癌症进展中起着至关重要的作用。我们旨在阐明METTL3和长链非编码RNA转移相关肺腺癌转录本1 （MALAT1）参与多发性骨髓瘤（MM）发病的机制。方法采集56例MM患者和42例健康供者骨髓标本，检测METTL3和MALAT1水平。METTL3和MALAT1之间的相互作用也被确定。将METTL3-和malat1相关寡核苷酸转染到RPMI8226和U266细胞中，探讨其在细胞生长中的作用。检测RPMI8226和U266细胞的凋亡、迁移、增殖和侵袭。结果MM患者METTL3和MALAT1水平升高，干扰METTL3或MALAT1可抑制RPMI8226和U266细胞的恶性行为。METTL3和MALAT1之间存在相互作用。MALAT1过表达逆转了METTL3干扰对肿瘤细胞恶性的抑制作用。结论mettl3通过增强MALAT1的表达促进MM的发展。

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Regulatory role of the METTL3/MALAT1 axis in multiple myeloma progression

Objective

Methyltransferase-like 3 (METTL3) plays a crucial role in cancer progression, both in m6A modification-dependent and −independent pathways. We aimed to elucidate the mechanism by which METTL3 and the long noncoding RNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) contribute to the pathogenesis of multiple myeloma (MM).

Methods

Bone marrow samples were collected from 56 patients with MM and 42 healthy donors, followed by assessment of METTL3 and MALAT1 levels. An interaction between METTL3 and MALAT1 was also identified. METTL3- and MALAT1-related oligonucleotides were transfected into RPMI8226 and U266 cells to explore their role in cell growth. Apoptosis, migration, proliferation, and invasion of RPMI8226 and U266 cells were assayed.

Results

Elevated METTL3 and MALAT1 levels were observed in patients with MM. Interference with METTL3 or MALAT1 inhibited the malignant behavior of RPMI8226 and U266 cells. There was an interaction between METTL3 and MALAT1. Overexpression of MALAT1 reversed the inhibitory effects of METTL3 interference on tumor cell malignancy.

Conclusion

METTL3 augments MM development by enhancing MALAT1 expression.

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来源期刊

Journal of Bone Oncology ONCOLOGY-

CiteScore

7.20

自引率

2.90%

发文量

审稿时长

34 days

期刊介绍： The Journal of Bone Oncology is a peer-reviewed international journal aimed at presenting basic, translational and clinical high-quality research related to bone and cancer. As the first journal dedicated to cancer induced bone diseases, JBO welcomes original research articles, review articles, editorials and opinion pieces. Case reports will only be considered in exceptional circumstances and only when accompanied by a comprehensive review of the subject. The areas covered by the journal include: Bone metastases (pathophysiology, epidemiology, diagnostics, clinical features, prevention, treatment) Preclinical models of metastasis Bone microenvironment in cancer (stem cell, bone cell and cancer interactions) Bone targeted therapy (pharmacology, therapeutic targets, drug development, clinical trials, side-effects, outcome research, health economics) Cancer treatment induced bone loss (epidemiology, pathophysiology, prevention and management) Bone imaging (clinical and animal, skeletal interventional radiology) Bone biomarkers (clinical and translational applications) Radiotherapy and radio-isotopes Skeletal complications Bone pain (mechanisms and management) Orthopaedic cancer surgery Primary bone tumours Clinical guidelines Multidisciplinary care Keywords: bisphosphonate, bone, breast cancer, cancer, CTIBL, denosumab, metastasis, myeloma, osteoblast, osteoclast, osteooncology, osteo-oncology, prostate cancer, skeleton, tumour.