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<p>Oral squamous cell carcinoma (OSCC) is an aggressive malignancy with poor prognosis and limited therapeutic options. Plasminogen activator, urokinase (PLAU) is emerged as a potential key player in OSCC by bioinformatics analysis, but its function in OSCC have not been explored. Therefore, this study investigates its role and mechanism in OSCC progression, with a focus on its interaction with the N6-methyladenosine (m<sup>6</sup>A) writer ZC3H13. Differentially expressed genes in OSCC were identified through analysis of GEO datasets. A candidate oncogene was subsequently selected based on Gene Ontology enrichment analysis and validated using qRT-PCR in patient samples. The role of PLAU was examined by CCK-8, EdU, and transwell assays. In vivo tumorigenicity was evaluated using xenograft models. The relationship amongst PLAU and ZC3H13 was analyzed through correlation analysis, MeRIP, RIP, qRT-PCR, immunoblotting and mRNA stability assays. Finally, rescue experiments were conducted to validate the interactions between ZC3H13 and PLAU. PLAU upregulated in OSCC was identified as a candidate oncogene based on bioinformatic analysis and mRNA expression profiling. PLAU silencing suppressed cell proliferation, migration, invasion, and tumor growth, whereas its overexpression produced the opposite effects. Furthermore, ZC3H13 was positively correlated with PLAU expression. ZC3H13 overexpression enhanced m<sup>6</sup>A levels of PLAU to increase PLAU expression and mRNA stability. In addition, ZC3H13 overexpression partially rescued the suppressive effects of PLAU silencing on OSCC cells. In summary, these results illustrate that ZC3H13-mediated m<sup>6</sup>A modification increases PLAU mRNA stability and expression, thereby enhancing OSCC progression.</p>

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PLAU regulated by a m6A writer ZC3H13 plays the oncogenic role in oral squamous cell carcinoma

  • 期刊论文

  • 发表日期：

    2025年12月8日

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  • Qingqing Cao

摘要

Oral squamous cell carcinoma (OSCC) is an aggressive malignancy with poor prognosis and limited therapeutic options. Plasminogen activator, urokinase (PLAU) is emerged as a potential key player in OSCC by bioinformatics analysis, but its function in OSCC have not been explored. Therefore, this study investigates its role and mechanism in OSCC progression, with a focus on its interaction with the N6-methyladenosine (m6A) writer ZC3H13. Differentially expressed genes in OSCC were identified through analysis of GEO datasets. A candidate oncogene was subsequently selected based on Gene Ontology enrichment analysis and validated using qRT-PCR in patient samples. The role of PLAU was examined by CCK-8, EdU, and transwell assays. In vivo tumorigenicity was evaluated using xenograft models. The relationship amongst PLAU and ZC3H13 was analyzed through correlation analysis, MeRIP, RIP, qRT-PCR, immunoblotting and mRNA stability assays. Finally, rescue experiments were conducted to validate the interactions between ZC3H13 and PLAU. PLAU upregulated in OSCC was identified as a candidate oncogene based on bioinformatic analysis and mRNA expression profiling. PLAU silencing suppressed cell proliferation, migration, invasion, and tumor growth, whereas its overexpression produced the opposite effects. Furthermore, ZC3H13 was positively correlated with PLAU expression. ZC3H13 overexpression enhanced m6A levels of PLAU to increase PLAU expression and mRNA stability. In addition, ZC3H13 overexpression partially rescued the suppressive effects of PLAU silencing on OSCC cells. In summary, these results illustrate that ZC3H13-mediated m6A modification increases PLAU mRNA stability and expression, thereby enhancing OSCC progression.