生物
多发性骨髓瘤
癌症研究
表达式(计算机科学)
细胞生物学
基因表达
基因表达调控
遗传学
基因
免疫学
计算机科学
程序设计语言
作者
Yan Xiao,Kang Xu,Zhijuan Xu,Shuang Cong,Binbin Lai,Hao Wu,Shujun Yang,Lixia Sheng,Keting Wang,Yuhan Zheng,Guifang Ouyang,Dan Yang
出处
期刊:Genomics
[Elsevier]
日期:2024-04-01
卷期号:: 110846-110846
标识
DOI:10.1016/j.ygeno.2024.110846
摘要
Period circadian regulator 3 (PER3) functions as a tumor suppressor in various cancers. However, the role of PER3 in multiple myeloma (MM) has not been reported yet. Through this study, we aimed to investigate the potential role of PER3 in MM and the underlying mechanisms. RT-qPCR and western blotting were used to determine the mRNA and protein expression levels of PER3. Glyoxylate reductase 1 homolog (GLYR1) was predicted to be a transcription factor of PER3. The binding sites of GLYR1 on the promoter region of PER3 were analyzed using UCSC and confirmed using luciferase and chromatin immunoprecipitation assays. Viability, apoptosis, and metathesis were determined using CCK-8, colony formation, TUNEL, and transwell assays. We found that PER3 expression decreased in MM. Low PER3 levels may predict poor survival rates; PER3 overexpression suppresses the viability and migration of MM cells and promotes apoptosis. Moreover, GLYR1 transcriptionally activates PER3, and the knockdown of PER3 alleviates the effects of GLYR1 and induces its malignant behavior in MM cells. To conclude, GLYR1 upregulates PER3 and suppresses the aggressive behavior of MM cells, suggesting that GLYR1/PER3 signaling may be a potential therapeutic target for MM.
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