Capn4 promotes non-small cell lung cancer progression via upregulation of matrix metalloproteinase 2

• Published in: Medical oncology (Northwood, London, England) London, England), 2015-03, Vol.32 (3), p.51-51, Article 51
• Main Authors: Gu, Jie, Xu, Feng-kai, Zhao, Guang-yin, Lu, Chun-lai, Lin, Zong-wu, Ding, Jian-yong, Ge, Di
• Format: Article
• Language: English
• Subjects: Aged; Calpain - genetics; Calpain - metabolism; Carcinoma, Non-Small-Cell Lung - metabolism; Carcinoma, Non-Small-Cell Lung - mortality; Carcinoma, Non-Small-Cell Lung - pathology; Cell Line, Tumor; Female; Gene Knockdown Techniques; Hematology; Humans; Internal Medicine; Lung cancer; Lung Neoplasms - metabolism; Lung Neoplasms - mortality; Lung Neoplasms - pathology; Lymphatic Metastasis; Male; Matrix Metalloproteinase 2 - metabolism; Medicine; Medicine & Public Health; Middle Aged; Oncology; Original Paper; Pathology; Prognosis; Up-Regulation
• ISSN: 1357-0560; 1559-131X
• DOI: 10.1007/s12032-015-0500-7

The expression of calpain small subunit 1 (Capn4) is correlated with the invasion of several types of tumors. However, the roles of Capn4 in non-small cell lung cancer (NSCLC) remain unclear. In this study, we found that the expression of Capn4 in NSCLC tissues was much higher than that in nontumorous samples. High levels of Capn4 expression were associated with lymph node metastasis and large tumor size in NSCLC patients. The 5-year overall survival rate in the Capn4 high group was significantly lower than that in the Capn4 low group. In multivariate analysis, Capn4 was identified as an independent prognostic factor for overall survival. Moreover, in an in vitro analysis, downregulation of Capn4 expression by siRNA suppressed the invasive potential of lung cancer cells. Finally, we demonstrated that Capn4 enhanced the invasion ability of lung cancer cells by upregulating the expression of matrix metalloproteinase 2. Our findings indicated that Capn4 may represent a potential therapeutic target and a novel prognostic marker of NSCLC.