Hsa-miR-141-3p as a modulator of ZBTB16 expression in cervical cancer pathogenesis

This research investigated the function of Zinc Finger and BTB Domain Containing 16 (ZBTB16) in cervical cancer (CESC), along with its regulatory mechanisms linked to specific miRNAs. ZBTB16 expression in CESC was explored using the GEPIA2 database. ZBTB16-associated miRNAs were predicted and their expression patterns investigated using the R language, based on the CESC dataset from the TCGA database. The study utilized univariate Cox regression to pinpoint clinical risk factors. Kaplan-Meier analysis was used to examine the prognostic value of ZBTB16 and associated miRNAs. The expression of ZBTB16 in CESC was investigated using immunohistochemical staining. Through functional experiments, including dual-luciferase reporter, RT-qPCR (Reverse Transcription-quantitative Polymerase Chain Reaction), and Western blot, we confirmed that hsa-miR-141-3p targets ZBTB16. Based on GEPIA2 database, the expression of ZBTB16 in CESC tumor specimens was significantly reduced compared to normal controls ( P < 0.05). Hsa-miR-141-3p, predicted as the top regulatory miRNA of ZBTB16, was upregulated in CESC ( P < 0.05). Using immunohistochemical staining, this study found that ZBTB16 was downregulated in cancer tissues compared to controls, while hsa-miR-141-3p was upregulated in cancer tissues ( P < 0.05). Dual luciferase reporter assays revealed that hsa-miR-141-3p mimics reduced ZBTB16 3’-UTR activity, while hsa-miR-141-3p inhibitors enhanced ZBTB16 3’-UTR activity. RT-qPCR and Western blot analysis revealed that compared with the control group, the hsa-miR-141-3p mimic group exhibited decreased ZBTB16 mRNA and protein expression, while the hsa-miR-141-3p inhibitor group demonstrated increased ZBTB16 mRNA and protein expression ( P < 0.05). This study found that ZBTB16 expression was reduced and hsa-miR-141-3p expression was elevated in cervical cancer tissues. Furthermore, cellular experiments confirmed that hsa-miR-141-3p binds to and negatively regulates ZBTB16, providing experimental evidence to support basic research into targeted therapies.