Oral oncology · 2025
Mechanism of action of BMI1 in the induction of partial EMT in tongue squamous cell carcinoma to promote metastasis.
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Huang Tianyue, Chen Yingluo, Zhang Huilian, Chen Zhong, Wu Yanfei, Cheng Jun, Zhang Yufang, Cai Yihuang, Liu Jiawei
Аннотация
OBJECTIVE: To investigate the regulatory role of stemness factor BMI1 in epithelial-mesenchymal transition (EMT) and metastasis of tongue squamous cell carcinoma (TSCC) METHODS: Clinical and mouse TSCC specimens were analyzed for BMI1/TGF-β1 expression via immunohistochemistry (IHC). In vitro studies used SCC-9 cells with independent knockdown of BMI1 or TGF-β1; Protein levels quantified by RT-qPCR, Western blot, and immunofluorescence. Migration capacity assessed by Transwell and wound healing assays.
RESULTS: BMI1 was significantly upregulated in human and murine TSCC tissues. TGF-β1 knockdown reduced both E-cadherin and N-cadherin expression. BMI1 knockdown increased TGF-β1 expression but induced accumulation of dysfunctional cytoplasmic SMAD complexes. Both knockdowns impaired cell migration.
CONCLUSIONS: BMI1 maintains a pro-metastatic partial EMT (pEMT) state in TSCC by regulating TGF-β1. BMI1 knockdown dysregulates TGF-β1/SMAD signaling, trapping cells in a hybrid phenotype with disrupted cadherin balance and suppressed collective migration.
RESULTS: BMI1 was significantly upregulated in human and murine TSCC tissues. TGF-β1 knockdown reduced both E-cadherin and N-cadherin expression. BMI1 knockdown increased TGF-β1 expression but induced accumulation of dysfunctional cytoplasmic SMAD complexes. Both knockdowns impaired cell migration.
CONCLUSIONS: BMI1 maintains a pro-metastatic partial EMT (pEMT) state in TSCC by regulating TGF-β1. BMI1 knockdown dysregulates TGF-β1/SMAD signaling, trapping cells in a hybrid phenotype with disrupted cadherin balance and suppressed collective migration.