Rac3 promotes proliferation and invasion of endometrial cancer through the AKT/mTOR signalling pathway
Rac3 is associated with the malignancy of various tumours, including endometrial cancer (EC). Silencing Rac3 has been shown to effectively enhance the sensitivity of EC cells to chemotherapeutic drugs. Nonetheless, the underlying mechanism is still unclear. Firstly, the association between Rac3 and EC was verified through the TCGA database. Subsequently, Ishikawa cell lines with Rac3 knockdown were constructed. The effects of Rac3 knockdown on the growth, migration and invasion of Ishikawa cells were assessed through clone formation experiments, CCK-8 experiments, flow cytometry, and Transwell experiments. Finally, qRT-PCR and WB experiments were conducted to initially explore the potential mechanism of action of Rac3 in the development of EC. Compared with normal tissues, the expression of Rac3 in EC tissues was significantly elevated, and this expression further increased with the aggravation of tumour. In Ishikawa cells with Rac3 knockdown, cell viability was significantly reduced, the apoptosis rate increased, and the invasion and migration abilities of the cells were inhibited. Correlation analysis of EC samples revealed a positive correlation between Rac3 and AKT2, AKT3 and mTOR. Additionally, WB and qRT-PCR also suggested that the mechanism of action of Rac3 in the development of EC may be related to the upregulation of AKT2, AKT3 and mTOR. Knockdown of Rac3 may inhibit the occurrence and development of EC, which is related to its inhibition of AKT2, AKT3 and mTOR. This discovery provides a theoretical basis for clinical screening of biomarkers for EC and the development of potential therapeutic targets.