Time-Dependent Loss of miR-548c-3p and Activation of E2F3/FOXM1 in Breast Cancer: In Vitro and TCGA-Based Evidence for a Post-Transcriptional Mechanism.
MicroRNAs are key post-transcriptional regulators in breast cancer, but their time-dependent dynamics and downstream oncogenic effects are not fully understood.
APA
Bozkurt B, Ayan D, Bulut SM (2026). Time-Dependent Loss of miR-548c-3p and Activation of E2F3/FOXM1 in Breast Cancer: In Vitro and TCGA-Based Evidence for a Post-Transcriptional Mechanism.. International journal of molecular sciences, 27(2). https://doi.org/10.3390/ijms27021052
MLA
Bozkurt B, et al.. "Time-Dependent Loss of miR-548c-3p and Activation of E2F3/FOXM1 in Breast Cancer: In Vitro and TCGA-Based Evidence for a Post-Transcriptional Mechanism.." International journal of molecular sciences, vol. 27, no. 2, 2026.
PMID
41596697
Abstract
MicroRNAs are key post-transcriptional regulators in breast cancer, but their time-dependent dynamics and downstream oncogenic effects are not fully understood. miR-548c-3p has been proposed as a tumor suppressor, yet its temporal behavior and impact on cell cycle drivers remain unclear. This study investigated the time-dependent expression of miR-548c-3p and its post-transcriptional regulation of E2F3 and FOXM1 in MCF-7 breast cancer cells. Cells were analyzed at multiple time points (2-72 h) by quantitative real-time PCR to assess dynamic changes in miR-548c-3p, E2F3, and FOXM1 mRNA levels. Bioinformatic validation using TCGA-BRCA datasets and public platforms evaluated gene expression, promoter methylation, and prognostic significance. miR-548c-3p showed a progressive time-dependent decline, with the lowest levels at 72 h, whereas E2F3 and FOXM1 were significantly upregulated over time, supporting a post-transcriptional derepression mechanism. TCGA-based analyses confirmed overexpression and hypomethylation of E2F3 and FOXM1 in breast cancer, particularly in triple-negative tumors, and high expression of both genes was associated with poor survival. These findings indicate that time-dependent loss of miR-548c-3p contributes to E2F3 and FOXM1 activation through a post-transcriptional regulatory mechanism, highlighting this miRNA-oncogene axis as a potential prognostic signature and therapeutic target in breast cancer.
MeSH Terms
Humans; MicroRNAs; Forkhead Box Protein M1; Female; Gene Expression Regulation, Neoplastic; Breast Neoplasms; MCF-7 Cells; E2F3 Transcription Factor; DNA Methylation; Prognosis; Promoter Regions, Genetic; Cell Line, Tumor