S100A6 promotes carcinogenesis of lung adenocarcinoma cells

In our previous studies, we observed increased plasma levels of S100 calcium-binding protein A6 (S100A6) in patients with non-small-cell lung cancer. In Calu-6 lung cancer cells, S100A6 acts as a tumor suppressor by inhibiting growth and enhancing apoptosis, with no significant effect on cell differentiation. In the present study, we used lung adenocarcinoma (LUAD) cell lines to confirm the function of S100A6 in this subtype of lung cancer. We selected the LUAD cell line H1975 with high S100A6 expression and PC9 with low S100A6 expression, further constructing H1975 cells transfected with siRNA (H1975/SiRNA) and PC9 cells transfected with overexpressed S100A6 plasmid (PC9/S100A6). Control groups included blank cells and empty vector-transfected cells (named as H1975/neo and PC9/neo respectively). Cell Counting Kit-8, wound-healing, transwell assays, flow cytometric analysis, and nude mouse tumorigenicity were used to detect the biological activities of cells, including proliferation, migration, invasiveness, apoptosis, cell cycle, and tumorigenicity. By comparing cell behavior among the three groups in the two cell lines (H1975, H1975/neo, and H1975/SiRNA; PC9, PC9/neo, and PC9/S100A6), we found an association between S100A6 overexpression and enhanced cell proliferation, migration, invasion, tumorigenicity, and decreased apoptosis. Therefore, S100A6 promotes carcinogenesis in LUAD cells. Our results, from two aspects, indicate that S100A6 has an upbeat influence on the biological characteristics of LUAD cell lines, playing an important role in tumorigenesis and progression of LUAD.