GLUT-1 participates in the promotion of LncRNA CASC9 in proliferation and metastasis of laryngeal carcinoma cells.

Increasing evidence indicates that long non-coding RNA (lncRNA) may play important roles in tumorigenesis. Increased lncRNA CASC9 occurs in laryngeal carcinoma, which accounts for 20% of all head and neck cancers, but its role in this disease remains unknown. Using quantitative reverse transcriptase PCR, we found higher expression of CASC9 and GLUT-1 in laryngeal carcinoma tissues and cells, compared to adjacent tissues and cells. A correlation analysis showed a positive relationship between CASC9 and GLUT-1 expression in laryngeal carcinoma tissues. An MTT assay of TU212 and Hep-2 cells showed increased cell proliferation after transfection with overexpressed CASC9 and decreased cell proliferation after transfection with silenced CASC9. A Transwell assay showed that overexpressing CASC9 increased and silencing CASC9 decreased cell migration of TU212 and Hep-2 cells. A flow cytometry assay showed that overexpressing CASC9 reduced and silencing CASC9 increased cell apoptosis. In other words, we found that overexpressing CASC9 increased cell proliferation and cell migration and decreased apoptosis both in TU212 and Hep-2 cells, whereas silencing CASC9 had the opposite effects. Moreover, overexpression vector of GLUT-1 was used to investigate the molecular mechanism of CASC9 in laryngeal carcinoma. The results showed that transfection with an overexpressed GLUT-1vector reversed the effects of silencing CASC9 on proliferation, migration, and apoptosis in TU212 and Hep-2 cells. In conclusion, our study of laryngeal carcinoma found that CASC9 was positively correlated with GLUT-1 expression and that CASC9 may promote proliferation and metastasis of laryngeal carcinoma cells by regulating GLUT-1.

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