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Background <p>Nasopharyngeal carcinoma (NPC) is a malignant head and neck cancer with high mortality and dismal prognosis. Emerging research have disclosed that circRNAs are crucial gene expression regulators engaged in tumor advancement. This work aspired to identify novel oncogenic circRNA driving NPC progression.</p> Methods <p>Bioinformatics analysis was performed to explore and predict underlying circRNA and downstream targets. Luciferase reporter assay was executed to check the binding relationship between these genes. Cell function tests were conducted using CCK-8, would healing, and flow cytometry. The stemness markers CD133, Nanog and Oct4 was detected via western blot.</p> Results <p>CircCENPM was notably enhanced in NPC. Silencing of circCENPM suppressed NPC cell growth, migration, and stemness in vitro, simultaneously impeded tumorigenesis of NPC in vivo. Moreover, circCENPM could interact with miR-362-3p, whereas miR-362-3p inhibitor apparently reversed the mitigated growth and stemness induced by circCENPM knockdown in NPC cells. Furthermore, BMI1 was identified to be the downstream target of miR-362-3p, and BMI1 introduction partially offset the anti-tumor function of miR-362-3p in NPC cells.</p> Conclusion <p>CircCENPM functioned as a carcinogenic driver and facilitated NPC growth and stemness via miR-362-3p/BMI1 regulatory network, which provided a potential biomarker and attractive target for NPC intervention and treatment.</p>

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CircCENPM serves as a CeRNA to aggravate nasopharyngeal carcinoma metastasis and stemness via enhancing BMI1

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年3月14日

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  • Rui Wang,
  • Fei Wang

摘要

Background

Nasopharyngeal carcinoma (NPC) is a malignant head and neck cancer with high mortality and dismal prognosis. Emerging research have disclosed that circRNAs are crucial gene expression regulators engaged in tumor advancement. This work aspired to identify novel oncogenic circRNA driving NPC progression.

Methods

Bioinformatics analysis was performed to explore and predict underlying circRNA and downstream targets. Luciferase reporter assay was executed to check the binding relationship between these genes. Cell function tests were conducted using CCK-8, would healing, and flow cytometry. The stemness markers CD133, Nanog and Oct4 was detected via western blot.

Results

CircCENPM was notably enhanced in NPC. Silencing of circCENPM suppressed NPC cell growth, migration, and stemness in vitro, simultaneously impeded tumorigenesis of NPC in vivo. Moreover, circCENPM could interact with miR-362-3p, whereas miR-362-3p inhibitor apparently reversed the mitigated growth and stemness induced by circCENPM knockdown in NPC cells. Furthermore, BMI1 was identified to be the downstream target of miR-362-3p, and BMI1 introduction partially offset the anti-tumor function of miR-362-3p in NPC cells.

Conclusion

CircCENPM functioned as a carcinogenic driver and facilitated NPC growth and stemness via miR-362-3p/BMI1 regulatory network, which provided a potential biomarker and attractive target for NPC intervention and treatment.