ArticleAsia-Pacific journal of clinical oncology2025
E2F4 Promotes Malignant Behaviors of Prostate Cancer Through Activating MUC1 Expression Transcriptionally.
Article in Asia-Pacific journal of clinical oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- PVT1 lincRNA signals an androgen-dependent transcriptional activation program of oncogenes in prostate cancer cells.International journal of cancer · 2026Article
- E2F4 Mediates Mitophagy to Inhibit Ferroptosis in Esophageal Cancer Cells by Activating GPR176.Human mutation · 2026Article
- E2F4 Promotes Malignant Behaviors of Prostate Cancer Through Activating MUC1 Expression Transcriptionally.Asia-Pacific journal of clinical oncology · 2025Article
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7 authors.
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Abstract
backgroundThe malignant features of prostate cancer (PC) threaten the patient's life. MUC1 was observably enhanced in PC. However, the reason for higher MUC1 expression in PC is still unclear and deserves to be further investigated.
methodsThe abundance of MUC1 and E2F4 was evaluated using RT-qPCR in PC patients and PC cells. Pearson correlation coefficient analyzed the relationship between E2F4 and MUC1 in tissues from PC patients. Malignant phenotypes were examined using clone formation, scratch tests, transwell, and flow cytometry. The JASPAR website, luciferase activity assay, and ChIP were employed for validating interplays between E2F4 and the MUC1 promoter.
resultsMUC1 and E2F4 were abnormally elevated in samples of PC patients and PC cells. MUC1 silencing resulted in suppression of growth and metastasis and promotion of cell apoptosis of PC cells. Additionally, E2F4 could provoke the transcriptional activity of MUC1 to enhance MUC1 expression. Furthermore, E2F4 knockdown inhibited malignant features of PC cells, which was abolished by MUC1 overexpression.
conclusionOur findings revealed that E2F4 silencing led to the suppression of growth and metastasis and the promotion of cell apoptosis of PC cells through reducing MUC1 expression, which offered targeting molecules for PC treatment.
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