SPARCL1 suppresses cell migration and invasion in renal cell carcinoma

Abstract

Previous studies have shown that the human SPARC-like 1 (SPARCL1) is crucial for human cancer migration and invasion. In the present study, the expression, biological function and possible molecular regulatory mechanisms of SPARCL1 were investigated in human renal cell carcinoma (RCC). The protein expression of SPARCL1 in cells was evaluated using western blot analysis and immunohistochemical staining in the tissue microarray. The effects of SPARCL1 on the biological behaviors of RCC cells were assessed using in vitro assays. The present study also provisionally investigated the role of SPARCL1 on the mitogen-activated protein kinase (MAPK) signaling pathway. The results revealed that the expression of SPARCL1 was decreased in the RCC cell lines examined and in the tissue microarray. The overexpression of SPARCL1 significantly inhibited cell migration and invasion, and this may have been due to the inactivation of p38/c-Jun N-terminal kinase (JNK)/extracellular signal-regulated kinase (ERK) MAPKs. The results showed that high expression levels of SPARCL1 offered potential as a useful prognostic factor in RCC. Taken together, the present study demonstrated that the expression of SPARCL1 was downregulated in RCC cells and tissues, however, the overexpression of SPARCL1 inhibited RCC cell migration and invasion. SPARCL1 also reduced the expression of phosphorylated p38/JNK/ERK MAPKs. These data suggested that increasing the protein expression level of SPARCL1 may be novel strategy for treating RCC.