Preferentially expressed antigen (PRAME) in melanoma belongs to the CTA gene family and is aberrantly expressed in various cancer types. Previous studies have found that PRAME is highly expressed in cervical cancer tissues but not in normal tissues. Here, researchers examined PRAME expression in cervical tissues and cells using immunohistochemistry (IHC), qRT-PCR, and Western blotting. CCK-8, BrdU, wound healing assays, Transwell assays, and flow cytometry were used to investigate the role of PRAME in regulating the malignant biological behavior of cervical cancer cells. IHC, qRT-PCR, and Western blotting results showed that PRAME is highly expressed in cervical cancer tissues and cells. Knockdown of PRAME attenuated the growth, migration, and invasion of C33A and SiHa cells, induced G0/G1 arrest, and increased apoptosis by regulating the Wnt/β-catenin signaling pathway. However, upregulation of PRAME exhibited the opposite effect, which was partially reversed by MSAB treatment. When PRAME is overexpressed by activating the Wnt/β-catenin signaling pathway, the growth rate of xenograft tumors is enhanced. In summary, PRAME is associated with the development and progression of cervical cancer mediated by the Wnt/β-catenin signaling pathway, suggesting that PRAME may be one of the factors regulating the development of cervical cancer and a potential therapeutic target.
The cell cycle distribution of PRAME-knockdown and PRAME-overexpressing cells was assessed with PI staining by using flow cytometry, and cell cycle profiles were fitted by Flowjo software. As shown in Figures 1A and 1B, PRAME knockdown cells were more likely to arrest in the G0/G1 phase than corresponding control cells, while the proportion of cells in the S phase was lower in the PRAME knockdown group than in the control group. Compared with the control group, PRAME overexpression reduced the arrest of cells in the G0/G1 phase in C33A and SiHa cells, while the proportion of cells in the S phase in PRAME-overexpressing C33A and SiHa cells was higher than in the control group (Figures 1C and 1D). This suggests that PRAME knockdown disrupts cell cycle progression, while PRAME overexpression reduces the arrest of cells in the G0/G1 phase.
Figure 1. The effect of PRAME expression on cell cycle distribution of C33A and SiHa cells. (Chen X, et al., 2023)