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Plumbagin-mediating GLUT1 suppresses the growth of human tongue squamous cell carcinoma.
Oral Diseases 2018 September
OBJECTIVE: The purpose of this study was to investigate the clinical and histopathological characteristics of GLUT1 in human tongue squamous cell carcinoma (TSCC) and the role of plumbagin (PLB)-mediating GLUT1 in the growth of TSCC.
SUBJECTS AND METHODS: Forty-five cases of TSCC samples were collected and the expression and location of GLUT1 was analyzed. The role and mechanism of PLB meditating GLUT1 in the inhibitory growth of human TSCC cell line CAL27 were investigated in vitro and vivo.
RESULTS: The expression of GLUT1 was observed in all samples of human TSCC by immunohistochemical staining. GLUT1 expression was significantly correlated with lymph node metastasis and clinical stage in TSCC. PLB treatment decreased cell viability and colony formation, and increased cell apoptosis in association with the downregulation of GLUT1 via inhibiting PI3K/Akt pathway in vitro and PLB suppressed tumor growth in correlation with downregulation of GLUT1, compared with control group in vivo.
CONCLUSIONS: The findings demonstrated a novel anti-cancer mechanism of PLB, inhibitory TSCC growth via suppressing PI3K/Akt/GLUT1 pathway, which will supply a theoretical basis for PLB to treat TSCC.
SUBJECTS AND METHODS: Forty-five cases of TSCC samples were collected and the expression and location of GLUT1 was analyzed. The role and mechanism of PLB meditating GLUT1 in the inhibitory growth of human TSCC cell line CAL27 were investigated in vitro and vivo.
RESULTS: The expression of GLUT1 was observed in all samples of human TSCC by immunohistochemical staining. GLUT1 expression was significantly correlated with lymph node metastasis and clinical stage in TSCC. PLB treatment decreased cell viability and colony formation, and increased cell apoptosis in association with the downregulation of GLUT1 via inhibiting PI3K/Akt pathway in vitro and PLB suppressed tumor growth in correlation with downregulation of GLUT1, compared with control group in vivo.
CONCLUSIONS: The findings demonstrated a novel anti-cancer mechanism of PLB, inhibitory TSCC growth via suppressing PI3K/Akt/GLUT1 pathway, which will supply a theoretical basis for PLB to treat TSCC.
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