Role of the Translin/trax Complex and the miR-143-3p–CDK1–MAD2L1 Axis in Cervical Cancer Cell Cycle Regulation

Recent studies suggest that the Translin/trax (TSN/TSNAX) complex regulates target gene expression by degrading pre-miRNA, but its specific mechanism in cervical cancer remains unclear. Based on differential gene expression analysis of TCGA database, this study revealed that differentially expressed genes in cervical cancer were significantly enriched in cell cycle regulatory pathways (p=1.14e-20) and miRNA metabolic pathways (p=3.41e-04), suggesting their joint involvement in carcinogenesis. Multi-algorithm integration (DESeq2/edgeR/limma) identified miR-143-3p as a core significantly downregulated miRNA (log2FC=-3.31, Padj=4.28e-06), with its target genes CDK1 and MAD2L1 markedly upregulated in tumor tissues, driving dysregulated G2/M phase transition (CDK1) and spindle assembly checkpoint anomalies (MAD2L1), respectively. To explore upstream regulation mechanisms, core components TSN and TSNAX of the Translin/trax complex were prioritized based on functional association scores from the GeneCards database. Although no significant transcriptional differences were observed, their protein functions may be mediated through post-translational modifications or complex stability. Mechanistically, Translin/trax likely inhibits miR-143-3p maturation through competitive binding, thereby relieving its translational repression on CDK1 and MAD2L1, ultimately facilitating cell cycle checkpoint evasion and chromosomal segregation errors. This study is the first to elucidate the cascade regulatory role of the Translin/trax–miR-143-3p–CDK1/MAD2L1 axis in cervical cancer, providing novel theoretical insights for targeted cell cycle intervention and combinatorial immunotherapy.