Study of the Role of E2F1 and TMEM132A in Prostate Cancer Development.

Objective: Identify transcription factors and target genes associated with prostate cancer, offering new therapy approaches.

Methods: Gene Set Enrichment Analysis (GSEA) investigates early 2 factor (E2F) transcription factor family roles in prostate cancer using the TCGA database. Survival analysis examined E2F factors and patient survival connections. Dataset analysis identified E2F1-involved key genes. Quantitative Real-time PCR (qPCR), which combines ultrasound-guided methods to collect clinical samples from prostate cancer patients, was utilized to determine the expression levels of E2F1 and its target genes in patient samples and cancer cells. The effect of E2F1 and its target gene expression alterations on prostate cell proliferation was examined utilizing the cell counting kit-8 (CCK8) technique. Double fluorescence enzyme experiment verified E2F1-target gene connections.

Results: E2F family genes induce prostate cancer and show correlated co-expression. E2F1, E2F2, E2F3, E2F5, and E2F7 were considerably over-expressed in prostate cancer tissues. While E2F4 and E2F6 were notably underexpressed, there was no statistically important change in the E2F8 expression between prostate cancer and surrounding tissues. High expression of E2F genes is associated with lower patient survival. The transmemrane protein 132 (TMEM132A) was identified as a key gene for E2F1 action and is associated with poor prognosis in patients. The essential gene for E2F1 function, TMEM132A, was discovered. According to the qPCR results, E2F1 and TMEM132A are considerably expressed in cancer cells and patient samples. Interfering with its expression significantly inhibited the proliferation ability of cancer cells. The double luciferase experiment showed that E2F1 regulates the expression level in phase by binding directly to the TMEM132A promoter.

Conclusions: The E2F transcription factor family induces prostate cancer and correlates with poor prognosis. E2F1 directly regulates TMEM132A by binding its promoter and controlling the degree of protein expression, thereby affecting cancer cell growth.