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The role of the SOX2 gene in cervical cancer: focus on ferroptosis and construction of a predictive model
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The role of the SOX2 gene in cervical cancer: focus on ferroptosis and construction of a predictive model
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Journal Article
The role of the SOX2 gene in cervical cancer: focus on ferroptosis and construction of a predictive model
2024
Overview
BackgroundThe intricate interplay between stemness markers and cell death pathways significantly influences the pathophysiology of cervical cancer. SOX2, a pivotal regulator of stem cell pluripotency, has recently been implicated in the modulation of ferroptosis, a specialized form of iron-dependent cell death, in cancer dynamics. This study delineates the role of SOX2 in the ferroptotic landscape of cervical carcinoma.ObjectiveTo delineate the association between SOX2 expression and ferroptosis in cervical cancer and develop a robust, SOX2-centric model for predicting prognosis and enhancing personalized treatment.MethodsA multidimensional approach integrating advanced bioinformatics, comprehensive molecular profiling, and state-of-the-art machine learning algorithms was employed to assess SOX2 expression patterns and their correlation with ferroptosis marker expression patterns in cervical cancer tissues. A prognostic model incorporating the expression levels of SOX2 and ferroptosis indicators was meticulously constructed.ResultsThis investigation revealed a profound and intricate correlation between SOX2 expression and ferroptotic processes in cervical cancer, substantiated by robust molecular evidence. The developed predictive model based on SOX2 expression exhibited superior prognostic accuracy and may guide therapeutic decision-making.ConclusionThis study underscores the critical role of SOX2 in orchestrating the ferroptosis pathway in cervical cancer and presents a novel prognostic framework. The SOX2-centric predictive model represents a significant advancement in prognosis evaluation, offering a gateway to personalized treatment for gynaecologic cancers.
Publisher
Springer Nature B.V
Subject
