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<p>Actin filament-associated protein 1 antisense RNA 1 (AFAP1-AS1) has been found to be closely associated with the initiation and progression of various tumors; however, its role in oral squamous cell carcinoma (OSCC) remains unclear. AFAP1-AS1 expression in OSCC cells was detected using qRT-PCR. The regulatory effects of AFAP1-AS1 on tumor cell proliferation, migration, and invasive capabilities were systematically evaluated through CCK-8 proliferation, colony formation, wound healing, and Transwell invasion assays. Flow cytometry was employed to quantitatively analyze its impact on cell cycle progression and apoptotic. Based on bioinformatics predictions, a dual-luciferase reporter system was utilized to validate the targeting interactions among AFAP1-AS1, miR-93-3p, and CCND1. Functional rescue experiments were conducted to elucidate the functional regulatory network among them. Furthermore, a xenograft tumor model in nude mice was employed to verify in vivo the promoting effect of AFAP1-AS1 on tumor growth. AFAP1-AS1 was significantly upregulated in OSCC cells. AFAP1-AS1 knockdown inhibited the malignant phenotypes of OSCC cells. Mechanistic studies revealed that AFAP1-AS1 could target miR-93-3p and regulate CCND1 expression, thereby influencing OSCC progression. Subcutaneous tumor model in mice further confirmed the in vivo relevance of the AFAP1-AS1/miR-93-3p/CCND1 axis. AFAP1-AS1 downregulation inhibited OSCC progression through the miR-93-3p/CCND1 axis.</p>

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AFAP1-AS1 regulates oral squamous cell carcinoma development through the miR-93-3p/CCND1 signaling pathway

  • 期刊论文

  • 发表日期：

    2026年4月10日

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  • Kuangzheng Li,
  • Chengwei Li,
  • Qian He,
  • Xiaosheng Fan,
  • Lili Xu,
  • Yixia Jiang

摘要

Actin filament-associated protein 1 antisense RNA 1 (AFAP1-AS1) has been found to be closely associated with the initiation and progression of various tumors; however, its role in oral squamous cell carcinoma (OSCC) remains unclear. AFAP1-AS1 expression in OSCC cells was detected using qRT-PCR. The regulatory effects of AFAP1-AS1 on tumor cell proliferation, migration, and invasive capabilities were systematically evaluated through CCK-8 proliferation, colony formation, wound healing, and Transwell invasion assays. Flow cytometry was employed to quantitatively analyze its impact on cell cycle progression and apoptotic. Based on bioinformatics predictions, a dual-luciferase reporter system was utilized to validate the targeting interactions among AFAP1-AS1, miR-93-3p, and CCND1. Functional rescue experiments were conducted to elucidate the functional regulatory network among them. Furthermore, a xenograft tumor model in nude mice was employed to verify in vivo the promoting effect of AFAP1-AS1 on tumor growth. AFAP1-AS1 was significantly upregulated in OSCC cells. AFAP1-AS1 knockdown inhibited the malignant phenotypes of OSCC cells. Mechanistic studies revealed that AFAP1-AS1 could target miR-93-3p and regulate CCND1 expression, thereby influencing OSCC progression. Subcutaneous tumor model in mice further confirmed the in vivo relevance of the AFAP1-AS1/miR-93-3p/CCND1 axis. AFAP1-AS1 downregulation inhibited OSCC progression through the miR-93-3p/CCND1 axis.