Panoply™ Human PRKCB Over-expressing Stable Cell Line

Although the incidence of cervical cancer has decreased in high-income countries due to the implementation of human papillomavirus (HPV) vaccination and screening strategies, it remains a serious public health problem and a threat to women's health in low-income countries. Here, researchers conducted comprehensive proteomic and genomic analyses of cervical cancer tumors from 139 Chinese women. Integrating proteomic and genomic analyses linked genetic abnormalities to downstream disease-related pathways and revealed a landscape of HPV-associated multi-omics changes. The study found that EP300 enhances the acetylation of FOSL2-K222, thereby accelerating the malignant proliferation of cervical cancer cells. Proteomic stratification divided patients into three subgroups with distinct characteristics in terms of prognosis, genetic alterations, immune infiltration, and post-translational modification regulation. Furthermore, PRKCB was identified as a potential biomarker associated with radiotherapy response in cervical cancer patients.

To investigate the function of PRKCB in cervical cancer cell growth, researchers performed CCK-8 assays. The results showed that the proliferation of PRKCB-overexpressing SiHa cells was inhibited (Figure 1h). In a xenograft model, tumors formed by PRKCB-overexpressing cells were smaller than those formed by control cells (Figure 1i-k). Notably, PRKCB overexpression significantly enhanced the cytotoxic effect of radiation and induced G2/M phase cell cycle arrest in SiHa cells, suggesting that PRKCB may enhance radiosensitivity by regulating cell cycle progression (Figure 1l, m). These data suggest that PRKCB may be a promising biomarker for predicting radiotherapy efficacy and may play a tumor-suppressive role in cervical cancer.

Figure 1. Validation of the radioresponse-related biomarker, PRKCB. (Yu J, et al., 2024)