Panoply™ Human SLC34A2 Knockdown Stable Cell Line

Solute carrier 34 A2 (SLC34A2) is a member of the SLC34 family, a class of phosphate transporters. SLC34A2 has been reported to play a key role in tumorigenesis and progression. However, the biological role of SLC34A2 in gliomas remains unknown. Here, researchers analyzed the expression patterns of SLC34A2 in clinical glioma tissues and cell lines. Results showed that SLC34A2 is universally overexpressed in glioma tissues and cell lines. To further investigate the role of SLC34A2 in glioma, researchers generated SLC34A2 knockdown glioma cell lines U251 and U87. Subsequent studies demonstrated that SLC34A2 knockdown inhibited cell proliferation and migration/invasion. SLC34A2 knockdown also suppressed the epithelial-mesenchymal transition (EMT) phenotype, as demonstrated by increased E-cadherin expression and decreased N-cadherin and fibronectin expression. Furthermore, SLC34A2 knockdown enhanced the sensitivity of U251 and U87 cells to temozolomide (TMZ). In vivo tumorigenesis experiments demonstrated that SLC34A2 knockdown inhibited tumor growth. Furthermore, SLC34A2 knockdown suppressed activation of the epidermal growth factor receptor (EGFR)/PI3K/AKT signaling pathway in U87 cells. The EGFR inhibitor GW2974 enhanced cell proliferation and migration/invasion abilities suppressed by SLC34A2 knockdown and enhanced the sensitivity of glioma cells to TMZ, which was enhanced by SLC34A2 knockdown. These findings suggest that SLC34A2 may be a new potential target for glioma therapy.

To verify the effects of SLC34A2 knockdown on cell migration and invasion, the researchers performed Transwell assays. Compared with control cells, the migration ability of SLC34A2 knockdown U251 and U87 cells was significantly reduced (Figures 1A and B). Consistently, SLC34A2 knockdown also inhibited the invasion ability of U251 and U87 cells (Figures 1C and D). Furthermore, the researchers used Western blot to examine the expression of E-cadherin, N-cadherin, and fibronectin, reflecting the epithelial-mesenchymal transition (EMT) process. In SLC34A2 knockdown U251 and U87 cells, E-cadherin expression was increased, while N-cadherin and fibronectin expression was decreased (Figures 1E and F), indicating that SLC34A2 knockdown can block the EMT process.

Figure 1. Effect of SLC34A2 knockdown on the migration/invasion and EMT process in glioma cells. (Bao Z, et al., 2019)