| Literature DB >> 33095415 |
Daichi Nishiyama1, Yoshiaki Chinen1,2, Reiko Isa1, Yuto Fujibayashi1, Saeko Kuwahara-Ota1, Junko Yamaguchi1, Tomoko Takimoto-Shimomura1, Yayoi Matsumura-Kimoto1, Taku Tsukamoto1, Yuji Shimura1, Tsutomu Kobayashi1, Shigeo Horiike1, Masafumi Taniwaki3, Hiroshi Handa4, Junya Kuroda5.
Abstract
Multiple myeloma (MM) is cytogenetically, genetically and molecularly heterogenous even among subclones in one patient, therefore, it is essential to identify both frequent and patient-specific drivers of molecular abnormality. Following previous molecular investigations, we in this study investigated the expression patterns and function of the Ewing sarcoma breakpoint region 1 (EWSR1) gene in MM. The EWSR1 transcriptional level in CD138-positive myeloma cells was higher in 36.4% of monoclonal gammopathy of undetermined significance, in 67.4% of MM patients compared with normal plasma cells, and significantly higher in ten human myeloma-derived cell lines (HMCLs) examined. EWSR1 gene knockdown caused growth inhibition with an increase of apoptotic cells in NCI-H929 and KMS-12-BM cells. Gene expression profiling using microarray analysis suggested EWSR1 gene knockdown caused transcriptional modulation of several genes associated with processes such as cell proliferation, cell motility, cell metabolism, and gene expression. Of particular, EWSR1 gene knockdown caused upregulation of let-7c and downregulation of its known targets K-RAS and AKT. Finally, our analysis using community database suggested that high EWSR1 expression positively associates with poor prognosis and advanced disease stage in MM. These findings suggest that EWSR1 overexpression is a pro-oncogenic molecular abnormality that may participate in MM progression.Entities:
Keywords: Cell motility; Cell proliferation; EWSR1; Multiple myeloma; microRNA
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Year: 2020 PMID: 33095415 DOI: 10.1007/s12185-020-03027-0
Source DB: PubMed Journal: Int J Hematol ISSN: 0925-5710 Impact factor: 2.490