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Ki-67 is one of the most useful markers to evaluate cell proliferative activity and has been widely used in tumor treatment and research. However, its role in human laryngeal carcinoma remains poorly defined. The aim of the present study was to investigate the expression of Ki-67 in human laryngeal squamous carcinoma and the effect of Ki-67 gene silencing by small interfering (si)RNA on the proliferation of human laryngocarcinoma HEp2 cells. Immunohistochemistry and reverse transcription-quantitative polymerase chain reaction were performed to examine the expression of Ki-67 in human laryngeal squamous carcinoma tissues and adjacent non-cancer tissues from 50 patients with laryngeal squamous carcinoma. RNA interference was used to knock down the expression of Ki-67 in the HEp2 cell line, and the proliferation of the treated cells was observed in vitro . Western blot analysis was used to determine the expression levels of epidermal growth factor receptor (EGFR) and E-cadherin in the treated cells. The expression of Ki-67 in the laryngeal squamous carcinoma tissues was significantly higher than that of the adjacent non-tumor tissues (P=0.028). The high expression of Ki-67 in cancer was significantly correlated with cervical lymph node metastasis and clinical outcomes (all P&lt;0.001). The silencing of Ki-67 resulted in the inhibition of proliferation of the HEp2 human laryngocarcinoma cells (P&lt;0.001). In addition, compared with the control group, the expression levels of EGFR and E-cadherin in the Ki-67 siRNA-treated cells were significantly decreased (P&lt;0.001) and increased (P&lt;0.001), respectively. These results suggested that Ki-67 is important in regulating the proliferation of human laryngocarcinoma HEp2 cells and that the mechanism may at least partially be associated with the upregulation of EGFR and the downregulation of E-cadherin. Overall, Ki-67 can be used as an important indicator for judging clinical progress and estimating prognosis in human laryngeal squamous carcinoma.

Ki-67 is overexpressed in human laryngeal carcinoma and contributes to the proliferation of HEp2 cells