ArticleJCI insight2021
PRR11 promotes ccRCC tumorigenesis by regulating E2F1 stability.
Article in JCI insight, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 13 citations in OpenAlex.
- PRR11 as a newly identified oncogenic driver in retinoblastoma.Science China. Life sciences · 2026Article
- USP43 promotes gemcitabine resistance by regulating cholesterol homeostasis through E2F1 stabilization in bladder cancer.Journal of experimental & clinical cancer research : CR · 2025Article
- Identification of KRBA2 as a probable prognostic biomarker correlated with immune infiltration in kidney clear cell carcinoma.Current urology · 2025Article
- PRR11 Promotes Bladder Cancer Growth and Metastasis by Facilitating G1/S Progression and Epithelial-Mesenchymal Transition.Cancer medicine · 2025Article
- FBXW7/GSK3β-mediated proline-rich 11 degradation promotes oxidative DNA damage and inhibits tumor progression in renal cell carcinoma.Theranostics · 2025Article
- A targetable PRR11-DHODH axis drives ferroptosis- and temozolomide-resistance in glioblastoma.Redox biology · 2024Article
- AURKB/CDC37 complex promotes clear cell renal cell carcinoma progression via phosphorylating MYC and constituting an AURKB/E2F1-positive feedforward loop.Cell death & disease · 2024Article
- Article
- Identification of the E2F1-RAD51AP1 axis as a key factor in MGMT-methylated GBM TMZ resistance.Cancer biology & medicine · 2023Article
- Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Proline rich 11 (PRR11), a novel tumor-related gene, has been identified in different tumors. However, the relevant biological functions of PRR11 in human clear cell renal cell carcinoma (ccRCC) have not been studied. In this study, we first identified PRR11 as a biomarker of ccRCC and predictor of poor prognosis by bioinformatics. Then, we showed that PRR11 silencing substantially reduced ccRCC cell proliferation and migration in vitro and in vivo. Importantly, we found that PRR11 induced the degradation of the E2F1 protein through its interaction with E2F1, and PRR11 reduced the stability of the E2F1 protein in ccRCC cells, thereby affecting cell cycle progression. Further results indicated that the downregulation of E2F1 expression partially reversed the changes in ccRCC cell biology caused by PRR11 deletion. In addition, we showed that PRR11 was a target gene of c-Myc. The transcription factor c-Myc may have promoted the expression of PRR11 in ccRCC cells by binding to the PRR11 promoter region, thereby accelerating the progression of ccRCC. In summary, we found that PRR11 served as an oncogene in ccRCC, and PRR11 reduced the protein stability of E2F1 and could be activated by c-Myc.
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