Panoply™ Human PAK1 Knockdown Stable Cell Line

Hepatocellular carcinoma (HCC) is one of the leading causes of cancer-related death. PAK1 plays a crucial role in various cancers. However, the role of PAK1 in HCC remains unclear. Here, researchers show that both PAK1 and Snail are upregulated in HCC cells. Knockdown of PAK1 inhibits the proliferation, migration, and invasion of HCC cells and promotes apoptosis. PAK1 knockdown also inhibits tumor growth in vivo. Mechanistically, PAK1 promotes the EMT process by targeting Snail. PAK1 knockdown inhibits the β-catenin signaling pathway, upregulates the expression of pro-apoptotic proteins, and downregulates the expression of proliferation-related proteins. Therefore, PAK1 promotes the EMT process by increasing Snail expression and promotes HCC progression by activating the β-catenin pathway.

To further determine the role of PAK1 in HCC, researchers investigated how PAK1 levels affect the survival of HCC cells. Through colony formation assays, researchers found that the number of colonies formed by PAK1-knockdown HCC cells was significantly reduced (Figure 1A-B), indicating that shPAK1 inhibited liver cancer cell proliferation. Furthermore, compared to the control group, apoptosis was significantly increased in PAK1-knockdown HCC cells. In SMC-7721 and Bel-7402 cells, PAK1 knockdown increased the apoptosis rate from 1.97% to 21.39% and from 1.83% to 28.24%, respectively (Figure 1C-D). Therefore, inhibiting PAK1 can suppress the proliferation of liver cancer cells while promoting their apoptosis.

Figure 1. Knockdown of PAK1 inhibited proliferation but promoted apoptotic death of HCC cells. (Cao F, Yin L X., 2020)