The Mechanism of Paired Box-1 in the Progression of Cervical Carcinoma

Abstract

Background: While the methylation status of the tumor suppressor Paired Box-1 (PAX1) is recognized as a cervical cancer diagnostic biomarker, PAX1s exact role is unclear. This study delves into PAX1s possible contribution to cervical cancer progression. Methods: We engineered overexpression of PAX1 in the human cervical cancer cell line, HeLa, via cell transfection. Quantitative reverse transcription-polymerase chain reaction evaluated PAX1 expression. The Cell Counting Kit-8 assay was employed to gauge cell proliferation, and apoptosis rates alongside cell cycles were determined by flow cytometry. Invasion and migration capacities were evaluated via transwell and wound healing assays. Differential gene expression and pathway analysis were conducted using bioinformatics tools, while the levels of PAX1 protein were quantified via Western blotting. Results: Cervical cancer cells were prevented from proliferation (p < 0.05), invasion (p < 0.01), and migration (p < 0.05) by overexpression of PAX1. The apoptosis rate of cervical cancer cells rose, and the cell cycle was restrained in the first gap (G1) phase after PAX1 transfection (p < 0.001). Furthermore, overexpression of PAX1 led to abnormal retinol metabolism in cervical cancer. Conclusions: PAX1 could potentially impede cervical cancer development by modulating retinol metabolism. This study could illuminate novel aspects of the progression pathways in cervical cancer.