Panoply™ Human LIFR Knockdown Stable Cell Line

Pancreatic cancer (PC) is one of the leading causes of cancer-related mortality worldwide. Frequent metastasis and recurrence are the main reasons for poor prognosis in PC patients. Therefore, the discovery of new biomarkers and a deeper understanding of the mechanisms of pancreatic tumorigenesis and metastasis are crucial. Here, researchers report that leukemia inhibitory factor receptor (LIFR) inhibits PC cell tumorigenesis and metastasis both in vitro and in vivo. LIFR expression is significantly reduced in PC tissues and correlates with local invasion, lymph node metastasis, and tumor node metastasis (TNM) stage. In vitro, LIFR overexpression significantly inhibits PC cell colony formation, migration, invasion, and wound repair, while LIFR silencing exhibits the opposite effect. Furthermore, animal xenograft and metastasis models confirm the in vivo and in vitro results. LIFR also inhibits the expression of β-catenin, vimentin, and slug, while inducing E-cadherin expression, suggesting a possible mechanism of action involving the epithelial-mesenchymal transition pathway and a negative regulatory role for LIFR in PC cell metastasis.

Clinical invasion characteristics of pancreatic cancer patients are closely correlated with LIFR expression levels, suggesting that LIFR may play a negative regulatory role in pancreatic cancer metastasis. To confirm the effect of LIFR on pancreatic cancer cell metastasis, researchers conducted Transwell migration and invasion assays. As shown in Figures 1A and B, LIFR-knockdown Capan-1 cells significantly enhanced their migration and invasion abilities. Conversely, overexpression of LIFR in pancreatic cancer cells significantly reduced the migration and invasion abilities of PATU-8988 cells. Furthermore, the researchers quantitatively investigated the effect of LIFR on cell migration using a wound wound assay. Compared with control cells, the distance between the scratch edges in LIFR-knockdown Capan-1 cells was significantly shortened (Figures 1E and 1G). Consistent with this, overexpression of LIFR in PATU-8988 cells prolonged the wound healing distance (Figures 1F and G). Taken together, these results demonstrate that the invasive and highly metastatic phenotype of PC cells can be regulated in vitro by LIFR.

Figure 1. LIFR negatively regulates the metastasis of PC cells in vitro. (Ma D, et al., 2016)