LAUSR

Objective Beclin1 was previously found to be downregulated in human laryngeal cancer (LC) tissues, and it results in poor prognosis. This study aimed to further confirm the antitumor effects of Beclin1 in LC cell line Hep-2. Materials and methods Beclin 1 was overexpressed in Hep-2 cells using liposomal transfection and confirmed using reverse transcription polymerase chain reaction and Western blotting. Then, cell proliferation and apoptosis were determined in control (untransfected), empty vector transfected, and Beclin1 overexpressed groups using MTT and flow cytometry procedure, respectively. Results The expression of the Beclin1 gene in Hep-2 cells was significantly increased after vector transfection compared with control (1.173±0.046 vs 0.453±0.016, P<0.01) and empty vector (1.173±0.046 vs 0.440±0.021, P<0.01). Overexpression of Beclin1 inhibited proliferation at 4 days (0.619±0.051 vs 0.891±0.081 and 0.619±0.051 vs 0.878±0.105, P<0.01), 5 days (0.684±0.078 vs 1.127±0.094 and 0.684±0.078 vs 1.162±0.117, P<0.01), and 6 days (0.725±0.069 vs 1.168±0.103 and 0.725±0.069 vs 1.194±0.097, P<0.01) and promoted apoptosis (14.48%±1.42% vs 4.07%±0.66% and 14.48%±1.42% vs 4.39%±0.80%, P<0.01) in Hep-2 cells in comparison with the control and empty vector groups, respectively. Conclusion Beclin1 may be an underlying target for the treatment of LC. This study has provided some experimental basis for the gene therapy of LC.