RAC1 promotes the occurrence and development of tongue squamous cell carcinoma by regulating RAC1/PAK1/LIMK1 signaling pathway

RAC1通过调控RAC1/PAK1/LIMK1信号通路促进舌鳞状细胞癌的发生和发展

阅读:1

Abstract

Tongue squamous cell carcinoma (TSCC) remains an unsolved medical problem due to its poor local recurrence rate and prognosis. The purpose of this study was to investigate the expression characteristics of RAC-related C3 botulinum toxin substrate 1(RAC1) in TSCCS and its role in tumor invasion and metastasis. In this study, immunohistochemical staining was used to detect RAC1 expression in 150 tongue cancer specimens. The correlation between RAC1 and clinical-pathological characteristics is analyzed, along with the association between protein levels and disease-specific survival, metastasis-free survival, and local recurrence-free survival. In vitro experiments, RAC1 was knocked down by short hairpin RNA transfection to reveal the role of RAC1 in the invasion and metastasis of TSCC. The regulatory effects of RAC1 on CAL27 cell migration and invasion were evaluated by scratch and invasion methods. The influence of RAC1 expression on tumor growth was scrutinized using a subcutaneous transplant model in nude mice. RAC1 is overexpressed in TSCC and positively correlates with tumor invasion and metastasis. Moreover, elevated RAC1 expression is associated with poorer differentiation. Survival analysis further indicates that high expression of RAC1 is linked to increased recurrence and metastasis rates, as well as poorer prognosis. Additionally, both in vivo and in vitro studies demonstrate that RAC1 may impact tumor progression by modulating the epithelial-mesenchymal transition process through the RAC1/PAK1/LIMK1 signaling pathways. RAC1 overexpression is closely related to the progression of TSCC, and may provide a new prognostic indicator and therapeutic target for tongue cancer.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。