GLYR1 transcriptionally regulates PER3 expression to promote the proliferation and migration of multiple myeloma

IF 3.4 2区生物学 Q2 BIOTECHNOLOGY & APPLIED MICROBIOLOGY Genomics Pub Date : 2024-05-01 DOI:10.1016/j.ygeno.2024.110846

Xiao Yan , Kaihong Xu , Zhijuan Xu , Cong Shi , Binbin Lai , Hao Wu , Shujun Yang , Lixia Sheng , Keting Wang , Yuhan Zheng , Guifang Ouyang , Di Yang

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Abstract

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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GLYR1 转录调节 PER3 的表达，促进多发性骨髓瘤的增殖和迁移。

周期昼夜节律调节因子3（PER3）在多种癌症中发挥着肿瘤抑制因子的作用。然而，PER3在多发性骨髓瘤（MM）中的作用尚未见报道。本研究旨在探讨 PER3 在 MM 中的潜在作用及其内在机制。研究采用 RT-qPCR 和 Western 印迹法测定 PER3 的 mRNA 和蛋白表达水平。据预测，乙醛酸还原酶1同源物（GLYR1）是PER3的转录因子。使用 UCSC 分析了 GLYR1 在 PER3 启动子区域的结合位点，并使用荧光素酶和染色质免疫共沉淀试验进行了确认。使用 CCK-8、菌落形成、TUNEL 和透孔试验测定了细胞的活力、凋亡和变态反应。我们发现，PER3 在 MM 中的表达量减少。PER3水平低可能预示着存活率低；PER3过表达会抑制MM细胞的活力和迁移，并促进细胞凋亡。此外，GLYR1 可转录激活 PER3，而 PER3 的敲除可减轻 GLYR1 的影响并诱导 MM 细胞的恶性行为。总之，GLYR1能上调PER3并抑制MM细胞的侵袭行为，这表明GLYR1/PER3信号转导可能是MM的潜在治疗靶点。

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来源期刊

Genomics 生物-生物工程与应用微生物

CiteScore

9.60

自引率

2.30%

发文量

260

审稿时长

60 days

期刊介绍： Genomics is a forum for describing the development of genome-scale technologies and their application to all areas of biological investigation. As a journal that has evolved with the field that carries its name, Genomics focuses on the development and application of cutting-edge methods, addressing fundamental questions with potential interest to a wide audience. Our aim is to publish the highest quality research and to provide authors with rapid, fair and accurate review and publication of manuscripts falling within our scope.