Panoply™ Human CD44 Over-expressing Stable Cell Line

As a cell surface protein involved in a variety of biological processes, CD44 is involved in glucose metabolism in prostate cancer cells, but its molecular mechanism of regulation needs to be further elucidated. Here, the researchers used QRT-PCR and Western blot to detect the expression levels of PDK1 and PFKFB4, key enzymes of glucose metabolism, in CD44 overexpressing LNCaP cells. PDK1 and PFKFB4 were knocked down in LNCaP and PC3 cells using shRNA, respectively, and then cell proliferation, invasion and migration experiments were performed. The study found that overexpression of CD44 increased the expression levels of PDK1 and PFKFB4 in LNCaP cells. Silencing PDK1 and PFKFB4 reduced the proliferation of prostate cancer cells and inhibited their invasion and migration abilities. In addition, CD44 inhibitors significantly reduced the glucose consumption of PC-3 cells, significantly increased their ROS levels, and enhanced the sensitivity of PC-3 cells to docetaxel. In summary, CD44 can regulate the invasive phenotype of prostate cancer cells by regulating the expression of PDK1 and PFKFB4. CD44 may become a new potential therapeutic target.

CD44 plays a crucial role in altered glucose metabolism. As a glycolysis regulator, the researchers investigated whether CD44 affects the expression of glycolytic enzymes involved in the Kreb's cycle. After CD44 knockdown by siRNA, the researchers found that the mRNA expression (Figure 1A) and protein expression (Figure 1B) of PDK1 and PFKFB4 in PC-3 cells were significantly reduced. Similarly, when CD44 was overexpressed in LNCaP cells, the mRNA levels of PDK1 and PFKFB4 were significantly increased compared with the blank control and negative control (Figure 1C), and the relative protein expression was also significantly increased (Figure 1D, 1E).

Figure 1. The relative expressions of PDK1 and PFKFB4 in mRNA and protein after CD44 knockdown in PC-3 cells and CD44 overexpression in LNCaP cells. (Li W, et al., 2017)