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极光激酶B通过调节脂肪酸代谢影响肾透明细胞癌的增殖。

AURKB affects the proliferation of clear cell renal cell carcinoma by regulating fatty acid metabolism.

作者信息

Yang Yang, Li Dan, Liu Zhigang, Zhou Kai, Li Wenxing, Yang Yanqi, Sun Ruifang, Li Yulong

机构信息

School of Public Health, Shaanxi University of Chinese Medicine, Xianyang, Shaanxi, 712046, China.

Department of Cell Biology and Genetics, Medical College of Yan'an University, Yan'an, Shaanxi, 716000, China.

出版信息

Discov Oncol. 2025 Jan 27;16(1):91. doi: 10.1007/s12672-024-01352-y.

DOI:10.1007/s12672-024-01352-y
PMID:39869264
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11772637/
Abstract

BACKGROUND

Clear cell renal cell carcinoma (ccRCC) is the most common subtype of kidney cancer with a high metastatic rate and high mortality rate. The molecular mechanism of ccRCC development, however, needs further study. Aurora kinase B (AURKB) functions as an important oncogene in various tumors; therefore, in the present study, we aimed to explore the mechanism by which AURKB affects ccRCC development.

METHODS

We performed bioinformatics analysis, CCK-8 assay, RNA sequencing, RT-PCR and Western blot to analyze the function and mechanism of AURKB in ccRCC.

RESULTS

TIMER2.0 showed that AURKB was overexpressed in Kidney Renal Clear Cell Carcinoma (KIRC), the UALCAN database showed the survival rate of KIRC patients with different expression levels of AURKB and different gender indicated in the same gender, high AURKB expression predicts lower survival rate. Silencing of AURKB expression inhibits the proliferation of ccRCC cells. RNA-seq data suggested that AURKB is involved in fatty acid metabolism. Silencing of AURKB inhibited the expression of fatty acid synthase (FASN). FASN is a key gene involved in fatty acid metabolism. TIMER2.0 showed that FASN is upregulated in KIRC. Silencing of FASN inhibited the proliferation of ccRCC cells.

CONCLUSIONS

AURKB induces the proliferation of ccRCC cells by regulating fatty acid metabolism.

摘要

背景

透明细胞肾细胞癌(ccRCC)是肾癌最常见的亚型,具有高转移率和高死亡率。然而,ccRCC发生发展的分子机制仍需进一步研究。极光激酶B(AURKB)在多种肿瘤中作为重要的癌基因发挥作用;因此,在本研究中,我们旨在探讨AURKB影响ccRCC发生发展的机制。

方法

我们进行了生物信息学分析、CCK-8检测、RNA测序、RT-PCR和蛋白质免疫印迹,以分析AURKB在ccRCC中的功能和机制。

结果

TIMER2.0显示AURKB在肾透明细胞癌(KIRC)中过表达,UALCAN数据库显示不同AURKB表达水平的KIRC患者在相同性别中的生存率,高AURKB表达预示较低的生存率。沉默AURKB表达可抑制ccRCC细胞的增殖。RNA测序数据表明AURKB参与脂肪酸代谢。沉默AURKB可抑制脂肪酸合酶(FASN)的表达。FASN是参与脂肪酸代谢的关键基因。TIMER2.0显示FASN在KIRC中上调。沉默FASN可抑制ccRCC细胞的增殖。

结论

AURKB通过调节脂肪酸代谢诱导ccRCC细胞增殖。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/16f6/11772637/4712a18fff1a/12672_2024_1352_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/16f6/11772637/246df911346e/12672_2024_1352_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/16f6/11772637/1045a1d23a46/12672_2024_1352_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/16f6/11772637/507de0642727/12672_2024_1352_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/16f6/11772637/4712a18fff1a/12672_2024_1352_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/16f6/11772637/246df911346e/12672_2024_1352_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/16f6/11772637/1045a1d23a46/12672_2024_1352_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/16f6/11772637/507de0642727/12672_2024_1352_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/16f6/11772637/4712a18fff1a/12672_2024_1352_Fig4_HTML.jpg

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