Multiple myeloma (MM) is an incurable disease characterized by malignant plasma cell clonal expansion in the bone marrow; therefore, inhibiting the proliferation of plasma cells is an important approach to overcome the progression of MM. Quercetin (Que) is a promising flavonoid with broad-spectrum anti-tumor activity against various cancers, including MM; however, the underlying mechanism is not yet understood. The present study aimed to reveal the gene expression profile of Que-treated MM cells and clarify its potential mechanism. The 30% inhibitory concentration (IC30) of Que against MM cells was calculated, and the proliferation rate was significantly reduced after Que treatment. Next, 495 dysregulated genes were identified via RNA sequencing in Que-treated MM cells. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes analyses indicated that the dysregulated genes were enriched in various apoptosis-related GO terms and amino acid metabolism-related pathways. qPCR validation showed that protein tyrosine phosphatase receptor-type R (PTPRR) had the highest verified log2 FC (abs) among the top 15 dysregulated genes. Overexpression of PTPRR increased the sensitivity of MM cells against Que, significantly inhibiting their proliferation and colony formation ability; silencing of PTPRR showed the opposite results. Furthermore, bioinformatics analyses and PPI network construction of PTPRR indicated that dephosphorylation of ERK might be the potential pathway for the PTPRR-induced inhibition of MM cell proliferation. In summary, our study identified the gene expression profile in Que-treated MM cells and demonstrated that the upregulation of PTPRR was one of the important mechanisms for the Que-induced inhibition of MM cell proliferation.

中文翻译：

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槲皮素通过上调 PTPRR 表达来抑制多发性骨髓瘤细胞的增殖。

多发性骨髓瘤（Multiple myeloma，MM）是一种以骨髓中恶性浆细胞克隆扩增为特征的不治之症；因此，抑制浆细胞增殖是克服MM进展的重要途径。槲皮素 (Que) 是一种很有前途的黄酮类化合物，对包括 MM 在内的各种癌症具有广谱抗肿瘤活性；然而，潜在的机制尚不清楚。本研究旨在揭示 Que 处理的 MM 细胞的基因表达谱并阐明其潜在机制。计算Que对MM细胞的30​​%抑制浓度（IC30），Que处理后增殖率显着降低。接下来，在 Que 处理的 MM 细胞中通过 RNA 测序鉴定了 495 个失调基因。基因本体论 (GO) 和京都基因和基因组百科全书分析表明，失调的基因富含各种凋亡相关的 GO 术语和氨基酸代谢相关的途径。qPCR 验证表明，蛋白酪氨酸磷酸酶受体 R 型 (PTPRR) 在前 15 个失调基因中具有最高验证的 log2 FC (abs)。PTPRR的过表达增加了MM细胞对阙的敏感性，显着抑制了其增殖和集落形成能力；PTPRR 的沉默显示了相反的结果。此外，PTPRR的生物信息学分析和PPI网络构建表明ERK的去磷酸化可能是PTPRR诱导的MM细胞增殖抑制的潜在途径。总之，