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Upregulation of CCT3 promotes cervical cancer progression through FN1

  • Authors:
    • Lei Dou
    • Xinxin Zhang
  • View Affiliations / Copyright

    Affiliations: Department of Gynecology, The First Hospital of China Medical University, Shenyang, Liaoning 110001, P.R. China, Department of Discipline Inspection Commission, China Medical University, Shenyang, Liaoning 110001, P.R. China
    Copyright: © Dou et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Article Number: 856
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    Published online on: October 14, 2021
       https://doi.org/10.3892/mmr.2021.12496
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Abstract

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.
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Copy and paste a formatted citation
Spandidos Publications style
Dou L and Zhang X: Upregulation of CCT3 promotes cervical cancer progression through FN1. Mol Med Rep 24: 856, 2021.
APA
Dou, L., & Zhang, X. (2021). Upregulation of CCT3 promotes cervical cancer progression through FN1. Molecular Medicine Reports, 24, 856. https://doi.org/10.3892/mmr.2021.12496
MLA
Dou, L., Zhang, X."Upregulation of CCT3 promotes cervical cancer progression through FN1". Molecular Medicine Reports 24.6 (2021): 856.
Chicago
Dou, L., Zhang, X."Upregulation of CCT3 promotes cervical cancer progression through FN1". Molecular Medicine Reports 24, no. 6 (2021): 856. https://doi.org/10.3892/mmr.2021.12496
Copy and paste a formatted citation
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Spandidos Publications style
Dou L and Zhang X: Upregulation of CCT3 promotes cervical cancer progression through FN1. Mol Med Rep 24: 856, 2021.
APA
Dou, L., & Zhang, X. (2021). Upregulation of CCT3 promotes cervical cancer progression through FN1. Molecular Medicine Reports, 24, 856. https://doi.org/10.3892/mmr.2021.12496
MLA
Dou, L., Zhang, X."Upregulation of CCT3 promotes cervical cancer progression through FN1". Molecular Medicine Reports 24.6 (2021): 856.
Chicago
Dou, L., Zhang, X."Upregulation of CCT3 promotes cervical cancer progression through FN1". Molecular Medicine Reports 24, no. 6 (2021): 856. https://doi.org/10.3892/mmr.2021.12496
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