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 and its target genes in patient samples and cancer cells. The effect of 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. , , , , and were considerably over-expressed in prostate cancer tissues. While and were notably underexpressed, there was no statistically important change in the expression between prostate cancer and surrounding tissues. High expression of genes is associated with lower patient survival. The transmemrane protein 132 () was identified as a key gene for action and is associated with poor prognosis in patients. The essential gene for function, , was discovered. According to the qPCR results, and 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 regulates the expression level in phase by binding directly to the promoter.

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