The Expression of Rap1B in tongue squamous cell carcinoma and its effects on cell proliferation, invasion and migration

doi:10.19438/j.cjoms.2026.03.004

Abstract

Abstract: PURPOSE: To investigate the expression of Ras-related protein 1B (Rap1B) in tongue squamous cell carcinoma (TSCC) and its correlation with clinicopathological parameters and patient prognosis, while examining the effects of Rap1B silencing on TSCC cell proliferation, apoptosis, invasion, migration, and epithelial-mesenchymal transition (EMT) through in vitro experiments, along with exploring the underlying molecular mechanisms. METHODS: Rap1B expression in TSCC tissues was initially assessed using the GEPIA database. Rap1B protein levels in tissues were determined by Western blot and immunohistochemistry (IHC). The association between Rap1B expression and clinicopathological features, as well as patients' prognosis, was statistically evaluated. Following silencing of Rap1B by small interfering RNA (siRNA), Western blotting was employed to quantify the expression levels of Rap1B, PI3K, Akt, phosphorylated Akt (p-Akt), mTOR, phosphorylated mTOR (p-mTOR), p70S6K, phosphorylated p70S6K (p-p70S6K), and EMT-related markers (E-cadherin, N-cadherin, Vimentin). Cellular viability, proliferation, apoptosis, invasion, and migration were evaluated through CCK-8 assay, EdU assay, flow cytometry, Transwell invasion assay, and wound healing assay, respectively. RESULTS: Rap1B exhibited high expression in TSCC tissues (P<0.05). Rap1B expression levels demonstrated significant correlations with clinical TNM stage, depth of tumor invasion, and cervical lymph node metastasis status in TSCC (P<0.05). After Rap1B silencing, the protein expression levels of PI3K, p-Akt, p-mTOR, p-p70S6K, N-cadherin, and Vimentin in the experimental group were markedly downregulated (P<0.05), whereas the expression of E-cadherin was significantly upregulated (P<0.05). Silencing of Rap1B resulted in a significant reduction in TSCC cellular viability, proliferation, invasion, and migration (P<0.05), concomitant with a significant elevation in the apoptosis rate (P<0.05). CONCLUSIONS: Rap1B is highly expressed in TSCC. It facilitates tumor cell proliferation, invasion, migration, and EMT, while inhibiting apoptosis, through modulation of the phosphorylation status of the PI3K/AKT/mTOR/p70S6K signaling pathway. Targeted silencing of Rap1B can significantly suppress these malignant biological behaviors, indicating that Rap1B holds potential as a candidate molecular target for precision therapy in TSCC.

Key words: Tongue squamous cell carcinoma, Rap1B, Proliferation, Invasion, Epithelial-mesenchymal transition

CLC Number:

R739.86

Xu Yong, Cui Qian, Shao Yu, Xu Jin, Yu Wenyuan, Chen Zhenggang. The Expression of Rap1B in tongue squamous cell carcinoma and its effects on cell proliferation, invasion and migration[J]. China Journal of Oral and Maxillofacial Surgery, 2026, 24(3): 223-233.

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