Asia-Pacific journal of clinical oncology · 2025
E2F4 Promotes Malignant Behaviors of Prostate Cancer Through Activating MUC1 Expression Transcriptionally.
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Cheng Long, Yang Haichao, Tan Shuoguo, Shi Chongjun, Zeng Fanfei, Yang Weizhong, Kong Weiqin
Аннотация
BACKGROUND: The 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.
METHODS: The 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.
RESULTS: MUC1 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.
CONCLUSION: Our 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.
METHODS: The 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.
RESULTS: MUC1 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.
CONCLUSION: Our 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.