Data of gene expressions induced by the interaction between Kupffer cells and cancer cells dependently on Dectin-2

Metastasis to distal organ is a fatal cause of cancer death and liver is one of the most common site of metastasis leading to bad prognosis. Although it has been known that innate immune cells play critical roles in the regulation of liver metastasis, how they control the tumor development is still largely unclear. We found that Dectin-2 (Clec4n), a C-type lectin receptor (CLR), suppresses liver metastasis and such Dectin-2-mediated anti-tumor rejection requires Kupffer cells, liver-residing macrophages, which express Dectin-2 dominantly in liver. We used microarray to examine comprehensive gene expressions induced by Dectin-2 when anti-tumoral Kupffer cells interact with cancer cells Kupffer cells isolated from naïve wild-type or Dectin-2 KO mice were co-cultured with SL4, mouse colon carcinoma cell line. Subsequently, total RNA was extracted from whole cells and analyzed by microarray. As controls, wild-ype and Dectin-2-deficient Kupffer cells were separately cultured from SL4 cells and each total RNA was mixed.