Panoply™ Human SOD1 Over-expressing Stable Cell Line

Superoxide dismutase 1 (SOD1) is a major antioxidant enzyme that plays a pro-tumorigenic role in various human cancers. Although SOD1 is highly expressed in many cancers, its clinical significance and function in non-small cell lung cancer (NSCLC)-particularly the epigenetic regulatory mechanisms governing its role in NSCLC initiation and progression-remain insufficiently understood. Here, researchers found that SOD1 is highly expressed in NSCLC cell lines and tissues. Further studies demonstrated that high SOD1 expression promotes the proliferation, invasion, and migration of NSCLC cells, whereas inhibiting SOD1 expression induces G1 phase cell cycle arrest and apoptosis. Additionally, miR-409-3p was found to suppress SOD1 expression and significantly counteract its pro-tumorigenic activity. Bioinformatics analysis revealed that SETDB1 (SET domain bifurcated histone lysine methyltransferase 1) is involved in the epigenetic regulation of miR-409-3p and SOD1 expression and function in NSCLC cells. These findings suggest that SOD1 is a promising potential therapeutic target for NSCLC.

Based on the finding of elevated SOD1 expression in non-small cell lung cancer (NSCLC) cell lines, researchers selected the cell lines with the highest (H460) and lowest (H1299) SOD1 expression levels to generate SOD1-knockdown and SOD1-overexpressing cell lines, respectively (Figures 1A, B). Compared with the control and normal groups, the proliferative capacity of SOD1-knockdown H460 cells was significantly reduced (Figure 1C). Conversely, the proliferative capacity of SOD1-overexpressing H1299 cells was significantly enhanced (Figure 1D). Transwell assay results demonstrated that SOD1 knockdown significantly inhibited the invasion and migration of H460 cells compared with the control and normal groups (Figure 1E). Conversely, SOD1 overexpression significantly enhanced the invasion and migration capabilities of H1299 cells (Figure 1F). Furthermore, compared with untreated control cells, SOD1 knockdown led to a significant increase in the proportion of early and late apoptotic H460 cells (Figure 1G). In contrast, the apoptosis rate was significantly reduced in SOD1-overexpressing H1299 cells (Figure 1H). Regarding the cell cycle, flow cytometry analysis revealed that SOD1 inhibition induced G1 phase arrest; compared with control H460 cells, the number of cells in the G1 phase increased significantly, while the number of cells in the S phase decreased significantly (Figure 1I). Conversely, SOD1 overexpression in H1299 cells promoted cell cycle progression, characterized by a decreased proportion of cells in the G1 phase and an increased proportion in the S phase (Figure 1J).

Figure 1. Regulation of NSCLC cell proliferation, invasion, metastasis, apoptosis, and the cell cycle by SOD1. (Liu S, et al., 2020)