Authors

Yongshou Liu, Bo Yue, Xiaodong Chen, Liting Wen, Dingjun Zha, Penggang Hu#

Departments

Department of Otolaryngology-Head and Neck Surgery, Xijing Hospital, Air Force Medical University, Xi'an, PR China

Abstract

Objective: To study the effect of the down-regulation of ECT2 expression by siRNA interference on apoptosis of laryngeal squamous cell carcinoma Hep-2 cells and its mechanism. 

Methods: A human laryngeal carcinoma Hep-2 cell line was harvested, passaged and divided into an ECT2siRNA transfection group, an NCsiRNA transfection group and a Hep-2 group. The mechanism of proliferation, apoptosis, migration and invasion of human laryngeal carcinoma Hep-2 cells was detected by the CCK-8 method, flow cytometry, Transwell chamber and Western blot. 

Results: The results of CCK-8 assay showed that the growth rate in the ECT2siRNA group was significantly slower than that of the NCsiRNA group and the Hep-2 group at 2d and 3d (P<0.05). The proliferation index of cells in the ECT2siRNA group was significantly lower than that of the NCsiRNA group and the Hep-2 group (P<0.05). The flow cytometry showed that the percentage of apoptotic cells in the ECT2siRNA group was significantly higher than that in the NCsiRNA group and the Hep-2 group (P<0.05). Transwell results showed that the number of transmembrane cells in the ECT2siRNA group was significantly lower than that in the NCsiRNA group and the Hep-2 group (P<0.05). The migration inhibition rate of the ECT2siRNA group was significantly higher than that of the NCsiRNA group (P<0.01). Western blot analysis showed that after down-regulating ECT2 in Hep-2 cells, the expression of cleaved caspase-3 in the ECT2siRNA group was significantly up-regulated and then induced apoptosis. 

Conclusion: Down-regulation of ECT2 expression by siRNA can promote the proliferation, apoptosis and migration of Hep-2 cells, and its apoptosis may be realised by promoting cleaved caspase-3 expression. 

Keywords

siRNA, ECT2 expression, laryngeal squamous cell carcinoma, Hep-2 cell, apoptosis, mechanism.

DOI:

10.19193/0393-6384_2020_3_259