Panoply™ Human PDGFB Knockdown Stable Cell Line

Radiotherapy is a primary and well-tolerated treatment modality for locally advanced esophageal squamous cell carcinoma (ESCC). However, there are currently no effective biomarkers for predicting the prognosis of ESCC patients. Platelet-derived growth factor (PDGF) has been associated with poor prognosis in various malignancies. In this study, researchers evaluated the impact of PDGF-BB on the efficacy of radiotherapy for ESCC and investigated the underlying mechanisms. Serum samples were collected from 68 patients undergoing neoadjuvant or definitive radiotherapy-both before and during treatment-and gene expression analysis results were validated using enzyme-linked immunosorbent assay (ELISA). The analysis revealed that patients who exhibited a significant decrease in PDGF-BB levels tended to have better progression-free and overall survival outcomes compared to other patients. Knockdown of PDGFB significantly inhibited cancer cell proliferation, invasion, and migration; furthermore, inhibiting PDGFB induced apoptosis and enhanced cellular sensitivity to ionizing radiation (IR). Additionally, IR inhibited PDGF-BB-induced cell migration by blocking the PI3K/AKT pathway in ESCC cells. These findings suggest that PDGF-BB expression levels serve as a potential indicator for predicting radiotherapy efficacy and assessing prognosis in patients with locally advanced ESCC undergoing radiotherapy.

Here, researchers investigated the effect of PDGFB on the radiosensitivity of KYSE30 and KYSE150 cells. Under different doses of radiation (2, 4, 6, and 8 Gy), PDGFB knockdown esophageal squamous cell carcinoma (ESCC) cells exhibited lower colony-forming ability compared to control cells (Figure 1A). This result indicates that inhibiting PDGFB can increase the radiosensitivity of ESCC cells. Furthermore, they further investigated the effect of PDGF-BB on ESCC cell migration and whether radiation irradiation (IR) interfered with it. The study found that PDGF-BB could induce ESCC cell migration. Under the same dose conditions, PDGF-BB increased the number of migrating cells. Meanwhile, when cells were exposed to increasing doses of radiation, the number of migrating cells was significantly reduced (Figure 1B). These results strongly suggest that PDGF-BB promotes the migration of KYSE30 and KYSE150 cell lines, while radiation irradiation inhibits this process. Furthermore, to further evaluate how radiation irradiation affects PDGF-BB-induced ESCC cell migration, researchers added PDGF-BB (50 ng/ml) to PDGFB- knockdown ESCC cells after irradiation (8 Gy) and collected the cells. They performed Western blot analysis to verify the correlation between protein expression and cellular responses to PDGF-BB and radiation pretreatment (Figure 1C). The results showed that in both KYSE30 and KYSE150 cell lines, the addition of PDGF-BB significantly activated the PI3K/AKT signaling pathway; while radiation pretreatment inhibited PDGF-BB-induced PI3K and AKT phosphorylation in both cell lines. Therefore, these results indicate that radiation irradiation inhibits PDGF-BB-induced cell migration by suppressing the PI3K/AKT signaling pathway in ESCC cells (Figure 1B).

Figure 1. Inhibition of PDGFB enhanced the sensitivity of esophageal squamous cell carcinoma cells to ionizing radiation (IR), a treatment modality that suppressed PDGF-BB-induced migration, and did so by blocking the PI3K/AKT pathway. (Er P, et al., 2020)