MTA1-DT promotes endometrial cancer growth by modulating G2/M-related gene transcription via PURα

In recent years, patients with early endometrial cancer (EC) can achieve a good prognosis through surgery. However, advanced and recurrent cases have still posed significant therapeutic challenges. This study aimed to investigate the biological function of long non-coding RNAs (lncRNAs) in EC and elucidate its underlying molecular mechanism. Through quantitative reverse transcription polymerase chain reaction (RT-qPCR) analysis, functional assays in cell lines, and bioinformatics approaches, we identified lncRNA MTA1-DT as a novel oncogenic factor in EC progression. RNA-seq and RT-qPCR analysis demonstrated that MTA1-DT was significantly upregulated with a 5-fold increase in EC cell lines compared to normal controls. Functional studies revealed that MTA1-DT promoted cell proliferation and migration. Mechanistically, we demonstrated that MTA1-DT physically interacted with purine-rich element binding protein-alpha (PURα) and facilitated its nuclear translocation, thereby enhancing its transcription factor activity. This nuclear accumulation of PURα promoted the transcription of downstream G2/M related genes, particularly EGF, leading to accelerated tumor growth. Thus, these results indicate that MTA1-DT exerts its oncogenic effects in EC through regulation of the cell cycle. Our findings establish MTA1-DT as a promising therapeutic target for EC treatment and provide new insights into the molecular mechanisms underlying EC progression.