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Cervical squamous cell carcinoma and endocervical adenocarcinoma (CESC) are major gynecological malignancies, causing significant cancer-related deaths in women. Current treatments yield poor outcomes, with a 5-year survival rate of only 17%. Identifying new biomarkers and therapeutic targets is crucial for improving prognosis and guiding personalized treatments.
We analyzed TCEAL2 expression using data from The Cancer Genome Atlas (TCGA) across various cancers, including CESC. We explored its correlation with clinical features, prognosis, immune infiltration, MSI, mRNAsi, and drug sensitivity. TCEAL2 expression was validated in GSE9750 datasets and CESC cell lines using qRT-PCR.
TCEAL2 expression was significantly dysregulated in CESC. Elevated TCEAL2 levels correlated with poor clinical outcomes, including advanced pathological M stage (p = 0.009), initial treatment failure (p = 0.0098), and reduced overall survival (OS) (p = 0.013). TCEAL2 was an independent predictor of unfavorable OS (p = 0.032). It was associated with key pathways such as calcium signaling, oxidative phosphorylation, and Wnt signaling. TCEAL2 also correlated with immune cell infiltration, MSI, and mRNAsi. Notably, TCEAL2 levels inversely correlated with sensitivity to several drugs, including CAY10603 and SB-223133.
The results suggest that TCEAL2 plays a significant role in CESC progression and its tumor microenvironment. Its correlation with immune infiltration and drug sensitivity highlights its potential as a prognostic biomarker and therapeutic target. Future studies should focus on elucidating the molecular mechanisms and validating their clinical utility.
TCEAL2 is a potential prognostic biomarker and therapeutic target in CESC. Further research is needed to explore its role and clinical applications.
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