m5C RNA甲基转移酶NOP2在高级别浆液性卵巢癌中的作用。

IF 4.4 4区 医学 Q2 ONCOLOGY
Cancer Biology & Therapy Pub Date : 2023-12-31 Epub Date: 2023-10-06 DOI:10.1080/15384047.2023.2263921
Shimin Yang, Dongmei Zhou, Chunxiao Zhang, Jiangdong Xiang, Xiaowei Xi
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引用次数: 0

摘要

核糖核酸甲基转移酶核仁蛋白p120(NOP2),通常被称为NOP2/Sun核糖核酸甲基转换酶家族成员1(NSUN1),参与细胞增殖,并在各种癌症中高度表达。然而,它在高级别癌症(HGSOC)中的作用尚不清楚。我们的研究调查了NOP2在HGSOC组织和正常伞组织中的表达,发现NOP2在HGSOC组织中显著上调。我们的实验表明,NOP2过表达在体内外促进了细胞增殖,并在体外增加了HGSOC细胞的迁移和侵袭能力。此外,我们确定Rap鸟嘌呤核苷酸交换因子4(RAPGEF4)是HGSOC中NOP2的潜在下游靶标。最后,我们的研究结果表明,NOP2和RAPGEF4的调节可能取决于m5C甲基化水平。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Function of m<sup>5</sup>C RNA methyltransferase NOP2 in high-grade serous ovarian cancer.

Function of m<sup>5</sup>C RNA methyltransferase NOP2 in high-grade serous ovarian cancer.

Function of m<sup>5</sup>C RNA methyltransferase NOP2 in high-grade serous ovarian cancer.

Function of m5C RNA methyltransferase NOP2 in high-grade serous ovarian cancer.

RNA methyltransferase nucleolar protein p120 (NOP2), commonly referred to as NOP2/Sun RNA methyltransferase family member 1 (NSUN1), is involved in cell proliferation and is highly expressed in various cancers. However, its role in high-grade serous ovarian cancer (HGSOC) remains unclear. Our study investigated the expression of NOP2 in HGSOC tissues and normal fimbria tissues, and found that NOP2 was significantly upregulated in HGSOC tissues. Our experiments showed that NOP2 overexpression promoted cell proliferation in vivo and in vitro and increased the migration and invasion ability of HGSOC cells in vitro. Furthermore, we identified Rap guanine nucleotide exchange factor 4 (RAPGEF4) as a potential downstream target of NOP2 in HGSOC. Finally, our findings suggest that the regulation of NOP2 and RAPGEF4 may depend on m5C methylation levels.

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来源期刊
Cancer Biology & Therapy
Cancer Biology & Therapy 医学-肿瘤学
CiteScore
7.00
自引率
0.00%
发文量
60
审稿时长
2.3 months
期刊介绍: Cancer, the second leading cause of death, is a heterogenous group of over 100 diseases. Cancer is characterized by disordered and deregulated cellular and stromal proliferation accompanied by reduced cell death with the ability to survive under stresses of nutrient and growth factor deprivation, hypoxia, and loss of cell-to-cell contacts. At the molecular level, cancer is a genetic disease that develops due to the accumulation of mutations over time in somatic cells. The phenotype includes genomic instability and chromosomal aneuploidy that allows for acceleration of genetic change. Malignant transformation and tumor progression of any cell requires immortalization, loss of checkpoint control, deregulation of growth, and survival. A tremendous amount has been learned about the numerous cellular and molecular genetic changes and the host-tumor interactions that accompany tumor development and progression. It is the goal of the field of Molecular Oncology to use this knowledge to understand cancer pathogenesis and drug action, as well as to develop more effective diagnostic and therapeutic strategies for cancer. This includes preventative strategies as well as approaches to treat metastases. With the availability of the human genome sequence and genomic and proteomic approaches, a wealth of tools and resources are generating even more information. The challenge will be to make biological sense out of the information, to develop appropriate models and hypotheses and to translate information for the clinicians and the benefit of their patients. Cancer Biology & Therapy aims to publish original research on the molecular basis of cancer, including articles with translational relevance to diagnosis or therapy. We will include timely reviews covering the broad scope of the journal. The journal will also publish op-ed pieces and meeting reports of interest. The goal is to foster communication and rapid exchange of information through timely publication of important results using traditional as well as electronic formats. The journal and the outstanding Editorial Board will strive to maintain the highest standards for excellence in all activities to generate a valuable resource.
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