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丝氨酸/苏氨酸蛋白激酶-3通过激活Ras-MAPK介导的细胞周期进程促进口腔鳞状细胞癌。

Serine/Threonine Protein Kinase-3 Promotes Oral Squamous Cell Carcinoma by Activating Ras-MAPK Mediated Cell Cycle Progression.

作者信息

Yue Li, Xu Yuedi, Lu Ping

机构信息

Department of Stomatology, Liaocheng People's Hospital, Liaocheng, Shandong, 252000, People's Republic of China.

出版信息

Int J Gen Med. 2023 Jul 21;16:3115-3124. doi: 10.2147/IJGM.S412155. eCollection 2023.

Abstract

PURPOSE

Serine/threonine protein kinase-3 (STK3) is a key molecule in the Hippo pathway, but its biological function in the development of oral squamous cell carcinoma (OSCC) remains unclear, we explored the roles of STK3 in OSCC.

METHODS

In this study, GEPIA was used to analyse STK3 expression in different types of tumor patients. OSCC patients were then collected from Liaocheng People's Hospital (Shandong, China), to further detect STK3 expression by qRT-PCR and Western blotting. To explore the function of STK3, overexpression and knockdown experiment were designed. Cell proliferation, migration and invasion were analyzed.

RESULTS

First, STK3 is significantly up-regulated in OSCC patients, and high STK3 expression is associated with poor prognosis. Then, in vitro cell proliferation, migration, and invasion tests were used to determine the role of STK3. STK3 overexpression significantly promoted the proliferation, migration and invasion of OSCC cells. The downregulation of STK3 inhibited the proliferation, migration and invasion of OSCC cells. Finally, STK3 was demonstrated to promote oral squamous cell carcinoma by activating Ras-MAPK mediated cell cycle progression.

CONCLUSION

The results showed that STK3 was a potential cancer promoter for OSCC. It plays an important role in promoting the progression of oral squamous cell carcinoma. Inhibition of STK3 may prove beneficial as a therapeutic strategy for OSCC treatment.

摘要

目的

丝氨酸/苏氨酸蛋白激酶-3(STK3)是Hippo信号通路中的关键分子,但其在口腔鳞状细胞癌(OSCC)发生发展中的生物学功能尚不清楚,我们对STK3在OSCC中的作用进行了探究。

方法

本研究利用GEPIA分析不同类型肿瘤患者中STK3的表达情况。随后从聊城市人民医院(中国山东)收集OSCC患者,通过qRT-PCR和蛋白质印迹法进一步检测STK3的表达。为探究STK3的功能,设计了过表达和敲低实验,并分析细胞增殖、迁移和侵袭情况。

结果

首先,STK3在OSCC患者中显著上调,且高表达的STK3与不良预后相关。然后,通过体外细胞增殖、迁移和侵袭试验确定STK3的作用。STK3过表达显著促进OSCC细胞的增殖、迁移和侵袭。STK3下调则抑制OSCC细胞的增殖、迁移和侵袭。最后,证实STK3通过激活Ras-MAPK介导的细胞周期进程促进口腔鳞状细胞癌。

结论

结果表明,STK3是OSCC潜在的癌症促进因子。它在促进口腔鳞状细胞癌进展中起重要作用。抑制STK3可能作为OSCC治疗的一种治疗策略而被证明是有益的。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e455/10368021/fef9938183d7/IJGM-16-3115-g0001.jpg

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