PRR11 Promotes Bladder Cancer Growth and Metastasis by Facilitating G1/S Progression and Epithelial-Mesenchymal Transition

Background

Although Proline-rich Protein 11 (PRR11) abnormalities are closely associated with carcinogenesis, the precise mechanism of bladder cancer remains unclear. Here, we sought to elucidate the molecular mechanisms of PRR11 in bladder cancer.

Methods

We performed differential expression analysis of PRR11 from the TCGA and GEO databases, followed by validation with clinical samples. Survival analysis was employed to assess the correlation between PRR11 and patient prognosis. The effects of PRR11 on bladder cancer cells were examined through both in vitro and in vivo experiments. Additionally, Gene Set Enrichment Analysis (GSEA) was used to predict the downstream pathways associated with PRR11, which were further validated through subsequent experiments.

Results

PRR11 is upregulated in bladder cancer and could lead to poor prognosis. In vitro, PRR11 promoted tumor cell proliferation; in vivo, it promoted subcutaneous tumor growth. PRR11 knockdown inhibited its oncogenic function. On the molecular level, PRR11 promotes tumor metastasis by inducing Epithelial-mesenchymal Transition (EMT). GSEA suggests that PRR11 is strongly linked to the cell cycle, and silencing of PRR11 can achieve anti-tumor effects by inhibiting CCNE and blocking the G1/S phase transition.

Conclusions

Our study demonstrates that silencing PRR11 can arrest the malignant progression of bladder cancer by inhibiting EMT and blocking the G1/S transition. Targeting PRR11 may provide new insights for targeting cell cycle therapy.