Expression of miR-195 in laryngeal squamous cell carcinoma and its effect on proliferation and apoptosis of Hep-2

Y. Shuang, C. Li, X. Zhou, Y.-W. Huang, L. Zhang

Department of Otorhinolaryngology and Maxillofacial Oncology; Tianjin Medical University Cancer Institute and Hospital, Key Laboratory of Cancer Prevention and Therapy, Tianjin Cancer Institute; National Clinical Research Center of Cancer; Tianjin, China. zhanglun_tijmu@163.com

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• Oncology

OBJECTIVE: To investigate the expression of miR-195 and its relationship with clinicopathological characteristics in laryngeal squamous cell carcinoma (LSCC), and to explore its effect and possible mechanism on proliferation and apoptosis of Hep-2.

PATIENTS AND METHODS: Real-time fluorescence quantitative PCR was used to detect the expression of miR-195 in laryngeal carcinoma tissues and adjacent normal tissues from 98 cases. Dual-luciferase reporter plasmid with Bcl-2 wild type and mutant type 3’ untranslated region was created to verify the target of miR-195 by luciferase assay. After Hep-2 cells were transfected with miR-195/Bcl-2, miR-195, Bcl-2 siRNA and negative control by lipofectamine, the protein expression of Bcl-2 was detected by Western blot analysis. The proliferation and apoptosis of Hep-2 were detected by MTS method and flow cytometry, respectively.

RESULTS: Compared with adjacent normal tissues, the expression of miR-195 was lower in laryngeal carcinoma tissues (p < 0.01). The low expression of miR-195 was positively correlated with distant metastasis and clinical stage (p < 0.05). The average survival time of patients with low expression was shorter than those with high expression by Kaplan-Meier method (p < 0.01). Multivariate Cox analysis showed that miR-195 expression and lymph node metastases were independent prognostic factors (p < 0.05).

CONCLUSIONS: The expression of miR-195 was significantly decreased in laryngeal carcinoma tissues, which was closely related to the clinicopathological characteristics of LSCC. miR-195 may inhibit the proliferation and promote the apoptosis of Hep-2 by regulating Bcl-2 expression, which as an anti-oncogene could have the potential to be a therapeutic strategy in the treatment of LSCC.

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