Association of OPN overexpression with tumor stage, differentiation, metastasis and tumor progression in human laryngeal squamous cell carcinoma.

Abstract

BACKGROUND:

Osteopontin (OPN) is overexpressed in many human tumors and involved in promotion of cancer cells by regulating various facets of tumor progression such as cell proliferation, invasion and metastasis. To understand roles of OPN in tumor progression of laryngeal squamous cell carcinoma (LSCC) or develop molecular marker for prognosis and treatment of LSCC, we thus explore biological function of OPN and correlation with p53 in LSCC.

METHODS:

The expression of OPN and p53 in tumor tissues of LSCC was determined immunohistochemically in both LSCC and adjacent normal tissues. Lentivirus vector with RNAi small hairpin gene sequence of OPN (named LV-shOPN) was transfected into Hep-2 cells. OPN expression was detected by Western blotting assay and the viability and invasive ability of Hep-2 cells were examined by MTS and transwell assay.

RESULTS:

We found that OPN and p53 protein expressions were significantly higher in LSCC tumor tissues than adjacent normal tissues (76.2% vs. 23.8% for OPN and 63.8% vs. 15.2% for p53, all P < 0.001). OPN expression was also significantly correlated with p53 expression, tumor stage, grade and the presence of lymph node. The constructed LV-shOPN effectively inhibited the OPN expression, viability and invasive ability of Hep-2 cells (all P < 0.050).

CONCLUSION:

Taken together, OPN is overexpressed in LSCC. OPN expression is correlated with p53 expression, tumor progression and lymph node metastasis. Additionally, RNAi silencing of OPN expression can significantly inhibit tumor viability and invasion ability of Hep-2 cells. Thus, OPN may be considered as a marker and potential gene targeting therapy in LSCC.

• Authors: Jianqiu Chen, Chunsheng Zhu, Zhen He, Min Geng, Guojun Li, Xiaofeng Tao, Fenghua Zhang
• Journal: International journal of clinical and experimental medicine (Int J Clin Exp Med) Vol. 8 Issue 5 Pg. 7116-24 ( 2015) ISSN: 1940-5901 [Print] United States
• PMID: 26221249 (Publication Type: Journal Article)