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<p>B-cell translocation gene 3 (<i>BTG3</i>), a tumor suppressor, is reduced in expression in several malignancies, including ovarian cancer, colorectal cancer, and gastric cancer, but its role in oral squamous cell carcinoma (OSCC) is unknown. This study aimed to investigate the expression of <i>BTG3</i> in OSCC, as well as explore its impact on the biological behavior of OSCC and the potential regulatory mechanisms. <i>BTG3</i> expression levels in OSCC and normal tissues were examined using the GEO database and the Kaplan-Meier Plotter database was used for survival analysis. Western blotting and quantitative real-time PCR were used to assess <i>BTG3</i> expression levels in OSCC tissues and neighboring normal tissues, as well as in oral epithelial cells (HOEC) and OSCC cell lines (CAL27 and SCC15). We found the expression level of <i>BTG3</i> was lower in OSCC tissues than in surrounding normal tissues, with higher expression indicating a better prognosis. In vitro assay demonstrated that overexpression of <i>BTG3</i> inhibited OSCC cell proliferation, migration, and invasion, resulting in cell cycle arrest at the G1 phase, as well as negatively regulating the PI3K/AKT signaling pathway and inhibiting EMT progression; knockdown had the opposite effect. <i>BTG3</i> represents a potential therapeutic target in OSCC treatment.</p>

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BTG3 suppresses oral squamous cell carcinoma progression by inhibiting PI3K/AKT signaling and EMT

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年3月17日

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  • Su Zhang,
  • Xi Chen,
  • Zhuang Liang,
  • Wei Wang,
  • Tenglong Hu

摘要

B-cell translocation gene 3 (BTG3), a tumor suppressor, is reduced in expression in several malignancies, including ovarian cancer, colorectal cancer, and gastric cancer, but its role in oral squamous cell carcinoma (OSCC) is unknown. This study aimed to investigate the expression of BTG3 in OSCC, as well as explore its impact on the biological behavior of OSCC and the potential regulatory mechanisms. BTG3 expression levels in OSCC and normal tissues were examined using the GEO database and the Kaplan-Meier Plotter database was used for survival analysis. Western blotting and quantitative real-time PCR were used to assess BTG3 expression levels in OSCC tissues and neighboring normal tissues, as well as in oral epithelial cells (HOEC) and OSCC cell lines (CAL27 and SCC15). We found the expression level of BTG3 was lower in OSCC tissues than in surrounding normal tissues, with higher expression indicating a better prognosis. In vitro assay demonstrated that overexpression of BTG3 inhibited OSCC cell proliferation, migration, and invasion, resulting in cell cycle arrest at the G1 phase, as well as negatively regulating the PI3K/AKT signaling pathway and inhibiting EMT progression; knockdown had the opposite effect. BTG3 represents a potential therapeutic target in OSCC treatment.