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RSK4对胃癌生物学特性的影响。

Effect of RSK4 on Biological Characteristics of Gastric Cancer.

作者信息

Hu Cong, Dai Jun, Lin Xu, Meng Ya, Liang Hui

机构信息

The First Department of General Surgery, Zhuhai People's Hospital, Jinan University, Zhuhai City, Guangdong Province, People's Republic of China.

Zhuhai Precision Medicine Research Center, Zhuhai People's Hospital, Jinan University, Zhuhai City, Guangdong Province, People's Republic of China.

出版信息

Cancer Manag Res. 2020 Jan 28;12:611-619. doi: 10.2147/CMAR.S238132. eCollection 2020.

DOI:10.2147/CMAR.S238132
PMID:32095082
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6995296/
Abstract

PURPOSE

Gastric cancer is one of the most common cancers with high mortality. Emerging evidences show that ribosomal s6 kinase4 (RSK4) may be an anti-oncogene in several types of cancers, while its function in GC is still unclear. In the present study, we investigated the role of RSK4 in GC progression using MGC-803 and HGC-27 cell lines in vitro and in vivo.

METHODS

The expression of RSK4 in gastric cancer cells was evaluated using RT-qPCR and Western blot analysis. We transfected cells with RSK4 siRNA to reduce the expression of RSK4 and then evaluated the effect of RSK4 on cellular function. MTT and cell cycle assays were used to study its effect on cell growth. Flow cytometry was used to evaluate cell apoptosis. Wound healing and Transwell assays were performed to investigate metastasis. Stable cell lines with or without RSK4 knockdown were constructed with lentivirus and tumor-bearing mice were used to investigate the effect of RSK4 on cancer progression.

RESULTS

The results revealed that reduction of RSK4 expression inhibited cell apoptosis and promoted cell proliferation, migration, and invasion. Additionally, RSK4 knockdown promoted tumorigenesis in vivo.

CONCLUSION

Our study demonstrated that RSK4 serves as a tumor suppressor in GC.

摘要

目的

胃癌是最常见且死亡率高的癌症之一。新出现的证据表明,核糖体S6激酶4(RSK4)在几种癌症中可能是一种抗癌基因,但其在胃癌中的功能仍不清楚。在本研究中,我们使用MGC - 803和HGC - 27细胞系在体外和体内研究了RSK4在胃癌进展中的作用。

方法

使用RT - qPCR和蛋白质印迹分析评估RSK4在胃癌细胞中的表达。我们用RSK4小干扰RNA转染细胞以降低RSK4的表达,然后评估RSK4对细胞功能的影响。MTT和细胞周期分析用于研究其对细胞生长的影响。流式细胞术用于评估细胞凋亡。进行伤口愈合和Transwell分析以研究转移情况。用慢病毒构建有或无RSK4基因敲低的稳定细胞系,并使用荷瘤小鼠研究RSK4对癌症进展的影响。

结果

结果显示,RSK4表达的降低抑制细胞凋亡并促进细胞增殖、迁移和侵袭。此外,RSK4基因敲低促进体内肿瘤发生。

结论

我们的研究表明,RSK4在胃癌中起肿瘤抑制作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ea59/6995296/49b45b6f85c3/CMAR-12-611-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ea59/6995296/8f29a07689a4/CMAR-12-611-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ea59/6995296/c39bab178294/CMAR-12-611-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ea59/6995296/5f824c50205e/CMAR-12-611-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ea59/6995296/49b45b6f85c3/CMAR-12-611-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ea59/6995296/8f29a07689a4/CMAR-12-611-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ea59/6995296/c39bab178294/CMAR-12-611-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ea59/6995296/5f824c50205e/CMAR-12-611-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ea59/6995296/49b45b6f85c3/CMAR-12-611-g0004.jpg

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本文引用的文献

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2
Global cancer statistics 2018: GLOBOCAN estimates of incidence and mortality worldwide for 36 cancers in 185 countries.全球癌症统计数据 2018:GLOBOCAN 对全球 185 个国家/地区 36 种癌症的发病率和死亡率的估计。
CA Cancer J Clin. 2018 Nov;68(6):394-424. doi: 10.3322/caac.21492. Epub 2018 Sep 12.
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Progress in the treatment of advanced gastric cancer.晚期胃癌治疗的进展
RSK4 转录本异构体在癌症中的差异表达及其临床相关性。
Int J Mol Sci. 2022 Nov 23;23(23):14569. doi: 10.3390/ijms232314569.
4
Raltitrexed regulates proliferation and apoptosis of HGC-27 cells by upregulating RSK4.雷替曲塞通过上调 RSK4 调节 HGC-27 细胞的增殖和凋亡。
BMC Pharmacol Toxicol. 2022 Aug 28;23(1):65. doi: 10.1186/s40360-022-00605-2.
5
FOXP2 regulates thyroid cancer cell proliferation and apoptosis via transcriptional activation of RPS6KA6.FOXP2通过转录激活RPS6KA6来调节甲状腺癌细胞的增殖和凋亡。
Exp Ther Med. 2022 Jun;23(6):434. doi: 10.3892/etm.2022.11361. Epub 2022 May 9.
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Epigenetic modification and BRAF gene mutation in thyroid carcinoma.甲状腺癌中的表观遗传修饰与BRAF基因突变
Cancer Cell Int. 2021 Dec 19;21(1):687. doi: 10.1186/s12935-021-02405-w.
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Tumour Biol. 2017 Jul;39(7):1010428317714626. doi: 10.1177/1010428317714626.
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