Upregulation of CCT3 promotes cervical cancer progression through FN1

The mechanisms underlying cervical cancer progression have not yet been fully elucidated; thus, further investigations are required. Chaperonin containing TCP1 subunit 3 (CCT3) expression was found to be upregulated in several types of human cancer. However, the roles of CCT3 in cervical cancer remain poorly understood. Thus, the present study aimed to determine the roles of CCT3 in the progression of cervical squamous cell carcinoma and endocervical adenocarcinoma (CESC). For this purpose, the Tumor Immune Estimation Resource and Gene Expression Profiling Interactive Analysis databases were used to analyze the mRNA and protein expression levels of CCT3 in CESC samples. The effects of CCT3 on the proliferation and migration of CESC in vitro were determined using various experiments, including proliferation, Transwell and flow cytometric assays. The results revealed that CCT3 expression was significantly upregulated in CESC, which was associated with a poor prognosis. The silencing of CCT3 suppressed CESC cell proliferation, migration and invasiveness in vitro. Additionally, CCT3-knockdown promoted CESC cell apoptosis and cell cycle arrest, and suppressed fibronectin 1 (FN1) protein expression. Furthermore, rescue assays demonstrated that CCT3 promoted CESC proliferation and migration via FN1. In conclusion, the findings of the present study demonstrated that CCT3 is closely associated with the progression of CESC. Thus, CCT3 may be considered a novel, promising biomarker, and a possible therapeutic target for CESC.

Automated summary

The study found that CCT3 expression was significantly upregulated in CESC, which was associated with a poor prognosis. Silencing CCT3 suppressed CESC cell proliferation, migration, and invasiveness in vitro. Additionally, CCT3-knockdown promoted CESC cell apoptosis, cell cycle arrest, and suppressed FN1 protein expression.