Renal cell carcinoma (RCC) is a common malignant tumor with poor prognosis and high mortality. The role of triggering receptor expressed on myeloid cells‑2 (TREM2) in RCC progression has been increasingly recognized, but its underlying mechanisms remain to be fully elucidated. Here, researchers evaluated the effects of TREM2 on RCC cells and its potential mechanisms. Results showed that TREM2 expression levels were significantly increased in cancerous tissues compared to adjacent normal tissues. CCK-8 and EdU assays indicated that TREM2 knockdown significantly inhibited RCC cell proliferation, while TREM2 overexpression promoted RCC cell proliferation. Scratch and Transwell assays showed that, compared to controls, TREM2 overexpression significantly enhanced RCC cell migration and invasion, while TREM2 knockdown significantly reduced RCC cell migration. Furthermore, Western blot analysis revealed that TREM2 knockdown in RCC cells significantly increased the phosphorylation levels of p53 and p21 proteins. In conclusion, TREM2 is highly expressed in RCC tissues and promotes RCC cell migration by inhibiting the p53 signaling pathway.
To assess the effect of TREM2 on renal cell carcinoma (RCC) cell migration, researchers conducted a scratch healing assay, observing wound healing at 0 and 24 hours. Compared to the sh-NC group, wound healing in the TREM2 knockdown ACHN cell line was significantly inhibited. Conversely, overexpression of TREM2 promoted wound healing in ACHN cells compared to the vector group (Figure 1A). These results indicate that TREM2 can enhance RCC cell migration. Transwell assays further showed that TREM2 knockdown significantly inhibited cell invasion compared to the sh-NC group, while overexpression of TREM2 significantly enhanced cell invasion compared to the vector group (Figure 1B). In summary, these results indicate that TREM2 promotes RCC cell migration and invasion.
Figure 1. TREM2 promotes migration of RCC cells. (Zhang L, et al., 2024)