{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Tang X"],"funding":["National Natural Science Foundation of China"],"pagination":["361"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8497505"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["6(1)"],"pubmed_abstract":["Multiple myeloma (MM) is an incurable plasma cell malignancy in the bone marrow characterized by chromosome instability (CIN), which contributes to the acquisition of heterogeneity, along with MM progression, drug resistance, and relapse. In this study, we elucidated that the expression of BUB1B increased strikingly in MM patients and was closely correlated with poor outcomes. Overexpression of BUB1B facilitated cellular proliferation and induced drug resistance in vitro and in vivo, while genetic targeting BUB1B abrogated this effect. Mechanistic studies unveiled that enforced expression of BUB1B evoked CIN resulting in MM poor outcomes mainly through phosphorylating CEP170. Interestingly, we discovered the existence of circBUB1B_544aa containing the kinase catalytic center of BUB1B, whic"],"journal":["Signal transduction and targeted therapy"],"pubmed_title":["BUB1B and circBUB1B_544aa aggravate multiple myeloma malignancy through evoking chromosomal instability."],"pmcid":["PMC8497505"],"funding_grant_id":["81970196","82073885"],"pubmed_authors":["Guo M","Gu C","Yang Y","Ke M","Gu X","Deng Z","Ding P","Lin Z","Zhou Y","Li M","Tang X","Yuan Y"],"additional_accession":[]},"is_claimable":false,"name":"BUB1B and circBUB1B_544aa aggravate multiple myeloma malignancy through evoking chromosomal instability.","description":"Multiple myeloma (MM) is an incurable plasma cell malignancy in the bone marrow characterized by chromosome instability (CIN), which contributes to the acquisition of heterogeneity, along with MM progression, drug resistance, and relapse. In this study, we elucidated that the expression of BUB1B increased strikingly in MM patients and was closely correlated with poor outcomes. Overexpression of BUB1B facilitated cellular proliferation and induced drug resistance in vitro and in vivo, while genetic targeting BUB1B abrogated this effect. Mechanistic studies unveiled that enforced expression of BUB1B evoked CIN resulting in MM poor outcomes mainly through phosphorylating CEP170. Interestingly, we discovered the existence of circBUB1B_544aa containing the kinase catalytic center of BUB1B, whic","dates":{"release":"2021-01-01T00:00:00Z","publication":"2021 Oct","modification":"2026-05-07T19:29:40.277Z","creation":"2022-02-11T12:03:51.935Z"},"accession":"S-EPMC8497505","cross_references":{"pubmed":["34620840"],"doi":["10.1038/s41392-021-00746-6"]}}