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.