Abstract
The main characteristics of cervical cancer are abnormal and uncontrolled cell proliferation, and it regulates cell growth, differentiation, and cell death through genetic and epigenetic changes. This paper mainly discusses the radiosensitivity of the cervical cancer protein kinase B signaling pathway and discusses the specific mechanisms that affect the occurrence and development of cervical cancer. In addition, this paper studies the effect of transient transfection knocking down the expression of TRIP4 in cervical cancer cells on the expression of key proteins in related signaling pathways and explores the mechanism of its specific effects and finds the mechanism of TRIP4's effect on cervical cancer radiosensitivity. The findings of this study show for the first time that knocking down TRIP4 inhibits cell viability by inhibiting the P13K/AKT and MAPK/ERK pathways, and this corresponds to the first part of the experimental results, which show that knocking down TRIP4 inhibits colony formation and increases apoptosis in HeLa and SiHa cells. Moreover, simultaneous inhibition of TRIP4 and hTERT proteins can increase the radiosensitivity of cervical cancer cells. These findings indicate that the inhibition of TRIP4 may be a new type of treatment that selectively targets the P13K/AKT and MAPK/ERK pathways and hTERT pathways in cervical cancer cells and provides a therapeutic option for the treatment of cervical cancer.
Highlights
Cervical cancer is the fourth most common cancer among women worldwide, and most cases occur in developing countries
We investigated the P13K/AKT and mitogenactivated protein kinase (MAPK)/ERK pathways in cervical cancer HeLa cell lines and SiHa cell lines in order to identify the particular mechanism of TRIP4 on cervical cancer, and we predicted that decreasing the production of the TRIP4 protein might block this route
We discovered that blocking this pathway may have an antitumor impact by reducing TRIP4 protein production and its underlying mechanism
Summary
Cervical cancer is the fourth most common cancer among women worldwide, and most cases occur in developing countries. Because the results of cytotoxic therapy are sometimes not satisfactory, new strategies for the treatment of cervical cancer are gradually turning to the study of targeted drugs, which are aimed at inhibiting specific molecules involved in tumor proliferation-related cellular pathways. In recent years, a new method for the treatment of cervical cancer has been proposed, that is, targeted drug therapy, whose purpose is to inhibit specific molecules involved in key cell pathways. Computational and Mathematical Methods in Medicine humanised monoclonal antibody that targets a circulating vascular endothelial growth factor It was authorised by the US FDA in 2014 as the first targeted medication for cervical cancer therapy (VEGF). Recent studies have shown that ASC-1 can play a role in the development of tumors and act as a coactivator of the transcription factors AP1, SRF, and NF-KB in HeLa cells. This article studies the radiosensitivity of the protein kinase B signaling pathway in cervical cancer to provide a theoretical reference for the treatment of cervical cancer
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