{"title":"METTL3/MALAT1轴在多发性骨髓瘤进展中的调节作用","authors":"Xiaohong Lu, Yafei Li, Ruie Li, Jingheng Zhang, Jiayu Peng, Yan Zhang","doi":"10.1016/j.jbo.2025.100695","DOIUrl":null,"url":null,"abstract":"<div><h3>Objective</h3><div>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).</div></div><div><h3>Methods</h3><div>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.</div></div><div><h3>Results</h3><div>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.</div></div><div><h3>Conclusion</h3><div>METTL3 augments MM development by enhancing MALAT1 expression.</div></div>","PeriodicalId":48806,"journal":{"name":"Journal of Bone Oncology","volume":"53 ","pages":"Article 100695"},"PeriodicalIF":3.4000,"publicationDate":"2025-06-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Regulatory role of the METTL3/MALAT1 axis in multiple myeloma progression\",\"authors\":\"Xiaohong Lu, Yafei Li, Ruie Li, Jingheng Zhang, Jiayu Peng, Yan Zhang\",\"doi\":\"10.1016/j.jbo.2025.100695\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><h3>Objective</h3><div>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).</div></div><div><h3>Methods</h3><div>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.</div></div><div><h3>Results</h3><div>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.</div></div><div><h3>Conclusion</h3><div>METTL3 augments MM development by enhancing MALAT1 expression.</div></div>\",\"PeriodicalId\":48806,\"journal\":{\"name\":\"Journal of Bone Oncology\",\"volume\":\"53 \",\"pages\":\"Article 100695\"},\"PeriodicalIF\":3.4000,\"publicationDate\":\"2025-06-12\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Journal of Bone Oncology\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/S2212137425000363\",\"RegionNum\":2,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q2\",\"JCRName\":\"Medicine\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Bone Oncology","FirstCategoryId":"3","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S2212137425000363","RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"Medicine","Score":null,"Total":0}
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.
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.