Depletion of the triggering receptor expressed on myeloid cells 2 inhibits progression of renal cell carcinoma via regulating related protein expression and PTEN-PI3K/Akt pathway.

The triggering receptor expressed on myeloid cells 2 (TREM-2) is suggested to be involved in the development of certain human malignancies. However, the functions of TREM-2 in renal cell carcinoma (RCC) are still less known. To reveal the effects of TREM-2 on the RCC progression, we examined the TREM-2 expression in RCC tumor tissues. Then, we analyzed the cell proliferation, cell apoptosis, cell cycle and expression of the relative factors in two selected RCC cell lines post RNA interference. We also analyzed the functions of TREM-2 in an in vivo nude mouse model. We found that, the expression of TREM-2 was abnormally elevated in RCC tumor tissues. Silencing TREM-2 inhibited cell growth, induced G1 phase arrest of cell cycle and cell apoptosis in RCC cells. In vivo, the results showed that depletion of TREM-2 significantly inhibited the ACHN tumor growth in the nude mouse model. The analysis of relative protein factors suggested that silencing TREM-2 downregulated the expression levels of Bcl2 and PCNA, and upregulated the expression levels of Bax and caspase-3 in RCC cell lines. Depletion of TREM-2 inactivated PI3K/Akt pathway through increasing the expression of PTEN. Taken together, TREM-2 acts as an oncogene in the development of RCC and can be considered as a novel therapeutic factor in the treatment of RCC.