ArticleFrontiers in oncology2021
Comprehensive Analysis of Cell Cycle-Related Genes in Patients With Prostate Cancer.
Article in Frontiers in oncology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 7 citations in OpenAlex.
- A severe neurodevelopmental syndrome linked to a South Asian founder variant in the UFMylation adaptor CDK5RAP3.Acta neuropathologica · 2026Article
- Integrative Analysis of Telomere-Related Genes Reveals Prognostic Signatures in Laryngeal Cancer.International journal of genomics · 2026Article
- Unveiling oncogene-induced senescence: a new frontier in prostate cancer prognosis and therapy.Discover oncology · 2025Article
- Single-Cell and Bulk RNA Sequencing Highlights Intra-Tumoral Heterogeneity and Malignant Progression Mechanisms in Prostate Cancer.Journal of cellular and molecular medicine · 2025Article
- Targeting WDR5/ATAD2 signaling by the CK2/IKAROS axis demonstrates therapeutic efficacy in T-ALL.Blood · 2025Article
- A cell cycle-related lncRNA signature predicts the progression-free interval in papillary thyroid carcinoma.Frontiers in endocrinology · 2023Article
- Construction of a DDR-related signature for predicting of prognosis in metastatic colorectal carcinoma.Frontiers in oncology · 2023Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This study aimed to identify critical cell cycle-related genes (CCRGs) in prostate cancer (PRAD) and to evaluate the clinical prognostic value of the gene panel selected. Gene set variation analysis (GSVA) of dysregulated genes between PRAD and normal tissues demonstrated that the cell cycle-related pathways played vital roles in PRAD. Patients were classified into four clusters, which were associated with recurrence-free survival (RFS). Moreover, 200 prognostic-related genes were selected using the Kaplan-Meier (KM) survival analysis and univariable Cox regression. The prognostic CCRG risk score was constructed using random forest survival and multivariate regression Cox methods, and their efficiency was validated in Memorial Sloan Kettering Cancer Center (MSKCC) and GSE70770. We identified nine survival-related genes: CCNL2, CDCA5, KAT2A, CHTF18, SPC24, EME2, CDK5RAP3, CDC20, and PTTG1. Based on the median risk score, the patients were divided into two groups. Then the functional enrichment analyses, mutational profiles, immune components, estimated half-maximal inhibitory concentration (IC50), and candidate drugs were screened of these two groups. In addition, the characteristics of nine hub CCRGs were explored in Oncomine, cBioPortal, and the Human Protein Atlas (HPA) datasets. Finally, the expression profiles of these hub CCRGs were validated in RWPE-1 and three PRAD cell lines (PC-3, C4-2, and DU-145). In conclusion, our study systematically explored the role of CCRGs in PRAD and constructed a risk model that can predict the clinical prognosis and immunotherapeutic benefits.
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