[Expression of Rho-related BTB domain-containing protein 1 in tongue squamous cell carcinoma and its effect on cell proliferation, invasion, and migration].

OBJECTIVES

This study explored the expression of Rho-related BTB domain-containing protein 1 (Rho-BTB1) in tongue squamous cell carcinoma (TSCC) cells; its effects on TSCC cell proliferation, invasion, and migration; and the underlying molecular mechanisms.

METHODS

RhoBTB1 expression in TSCC was analyzed by querying a bioinformatics online database. Forty-five cases of primary TSCC lesions resected during oral and maxillofacial surgery from December 2024 to August 2025 were selected. Immunohistochemistry and Western blot were used to detect RhoBTB1 expression in TSCC tissues and adjacent tissues. Two kinds of TSCC cell lines, CAL-27 and SCC-25, were selected for in vitro experiments. The overexpression plasmid vector and small interfering RNA were designed on the basis of the RhoBTB1 gene sequence. TSCC cells were transiently transfected, and the transfection efficiency was evaluated by real-time quantitative polymerase chain reaction. The proliferation, invasion, migration, and apoptosis of TSCC cells were evaluated by CCK-8 assay, Transwell cell invasion assay, cell scratch assay, and flow cytometry respectively. The expression levels of RhoBTB1, Rho-related protein kinase 1 (ROCK1), phosphatase and tensin homologue (PTEN), phosphorylated phosphatase and tensin homologue (p-PTEN), protein kinase B (AKT), and phosphorylated protein kinase B (p-AKT) were analyzed by Western blot. SPSS 22.0 and GraphPad Pri 8.0 were used to analyze the experimental data.

RESULTS

RhoBTB1 expression in TSCC tissues was significantly lower than that in adjacent tissues (P<0.05). RhoBTB1 overexpression significantly inhibited the proliferation, invasion, and migration of TSCC cells, promoted their apoptosis, down-regulated ROCK1/p-AKT, and up-regulated p-PTEN (P<0.05); no significant difference in expression was observed between PTEN and AKT (P>0.05). Knockdown of RhoBTB1 yielded opposing effects, with the upregulation of ROCK1 and p-AKT and the downregulation of p-PTEN (P<0.05). No significant differences were observed in the expression levels of PTEN and AKT (P>0.05).

CONCLUSIONS

RhoBTB1 is lowly expressed in TSCC and may inhibit its malignant phenotype by negatively regulating the ROCK1/PTEN/AKT pathway, suggesting its potential as an oncogene and therapeutic target.