ArticleFrontiers in oncology2026
TET1 loss promotes malignant phenotypes in HeLa cells and is associated with altered PTEN-PI3K/AKT/mTOR signaling.
Article in Frontiers in oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Objective: To investigate the biological significance of ten-eleven translocation 1 (TET1) in cervical cancer and its association with PTEN-PI3K/AKT/mTOR signaling. Methods: Publicly available bulk and single-cell transcriptomic datasets were analyzed, with histology-restricted analyses focused on cervical squamous cell carcinoma (SCC). TET1 immunoreactivity was assessed in five paired cervical adenocarcinoma and adjacent non-neoplastic tissues using nuclear H-scores. TET1 loss of function was modeled in HeLa cells by shRNA-mediated knockdown, with Bobcat339 used as a complementary TET-family inhibitor. Cellular metabolic activity, clonogenicity, cell-cycle distribution, apoptosis, migration, and invasion were evaluated using CCK-8, colony-formation, flow-cytometric, wound-healing, and Transwell assays. Protein expression and phosphorylation were examined by western blotting. Results: SCC-restricted bulk analyses consistently showed lower TET1 expression in cervical SCC than in normal cervical tissues. In TCGA-CESC SCC, TET1 expression was not significantly associated with PTEN expression or the PI3K-AKT-mTOR transcriptional score after multiple-testing correction, whereas an inverse association with the apoptosis score remained significant. Patient-level pseudobulk analysis of 12 SCC cases likewise identified no pathway association that remained significant after false-discovery-rate correction. In five paired cervical adenocarcinoma cases, TET1 nuclear H-scores were lower in all tumor samples than in their matched adjacent tissues, although the difference did not reach statistical significance (exact P = 0.0625). In HeLa cells, TET1 depletion increased cellular metabolic activity and clonogenicity, altered cell-cycle distribution, reduced apoptosis, and enhanced migration and invasion. These changes were accompanied by reduced PTEN expression and increased phosphorylation of PI3K, AKT, and mTOR. Conclusion: Reduced TET1 expression was observed in SCC-restricted public cohorts, while TET1 depletion promoted malignant phenotypes in HeLa cells. The accompanying changes in PTEN expression and PI3K/AKT/mTOR phosphorylation identify a candidate signaling association that warrants validation through rescue experiments and locus-specific epigenetic studies.
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