S100A6 can regulate cell proliferation, differentiation, cell cycle and apoptosis by interacting with target proteins under the condition of calcium ion existence. S100A6 gene is highly expressed in multiple tumor tissues and is closely related to the occurrence and development of tumor. The aim of this study is to explore the influence of S100A6 gene down-regulation on growth and apoptosis of transplanted lung adenocarcinoma in nude rats.

Eighteen healthy male Balb/c nude mice were randomly divided into three groups: empty vector control group (n=6), negative control group (n=6) and S100A6 gene RNA interference (RNAi) group (n=6). The transplanted lung adenocarcinoma models were established by subcutaneous injection of A549 lung adenocarcinoma cells line with empty vector, non-carrier vector and pLenR-GPH-shRNAi-S100A6, respectively. The growth of transplanted tumor in different groups was observed. The expression of S100A6 gene was detected using real-time PCR, immunohistochemistry and western-blot methods. Apoptosis cells were analyzed by Terminal-deoxynucleoitidyl transferase mediated nick end labeling (TUNEL).

The transplanted lung adenocarcinoma models in nude rat were successfully established. The pathological features showed that typical tumor cells formed solid hest-like mass. The tumor cell nucleus in empty vector control group and negative control group got bigger. The tumor cells in S100A6 RNAi group were relatively looser and their interstitial components became obvious. The tumor volume and mass among three groups had significant difference(P<0.05). The expression of S100A6 gene of RNAi group was significantly lower than that of empty vector control group and negative control group(P<0.05). The apoptosis rate had significantly difference among three groups(P<0.05). The nucleus of apoptosis cell in transplanted lung adenocarcinoma showed brown.

Down-regulation expression of S100A6 in lung adenocarcinoma could inhibit tumor growth and induce cell apoptosis, which could provide new pathway for further study of molecular target spot of lung adenocarcinoma.