Lu Xiaohong, Li Yafei, Li Ruie, Zhang Jingheng, Peng Jiayu, Zhang Yan
Department of Oncology, Luzhou People's Hospital, Luzhou 646000 Sichuan Province, China.
J Bone Oncol. 2025 Jun 12;53:100695. doi: 10.1016/j.jbo.2025.100695. eCollection 2025 Aug.
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).
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.
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.
METTL3 augments MM development by enhancing MALAT1 expression.
甲基转移酶样3（METTL3）在癌症进展中起着关键作用，涉及m6A修饰依赖性和非依赖性途径。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）促进多发性骨髓瘤（MM）发病机制的机制。
收集56例MM患者和42例健康供者的骨髓样本，随后评估METTL3和MALAT1水平。还鉴定了METTL3与MALAT1之间的相互作用。将与METTL3和MALAT1相关的寡核苷酸转染到RPMI8226和U266细胞中，以探讨它们在细胞生长中的作用。检测RPMI8226和U266细胞的凋亡、迁移、增殖和侵袭情况。
在MM患者中观察到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与MALAT1之间存在相互作用。MALAT1的过表达逆转了METTL3干扰对肿瘤细胞恶性程度的抑制作用。
METTL3通过增强MALAT1表达促进MM发展。
