Current evidence supports evaluation of CCAT2 in prostate cancer progression biomarker development and treatment resistance

Prostate cancer remains a major clinical challenge because of its molecular heterogeneity, metastatic progression, and development of treatment resistance. Long non-coding RNAs have emerged as regulators of tumor biology, and colon cancer-associated transcript 2 (CCAT2) has been investigated as a candidate oncogenic lncRNA in prostate cancer. Current prostate cancer-specific evidence most strongly supports increased CCAT2 expression, its association with unfavorable clinical outcomes, and its effects on proliferation, migration, invasion, and epithelial–mesenchymal transition-associated markers in established cell-line models and a single retrospective tissue cohort. VIRMA-dependent N6-methyladenosine modification may contribute to CCAT2 stability and abundance. In contrast, proposed links to MYC/Wnt/β-catenin signaling, chromosomal instability, metabolic reprogramming, angiogenesis, immune modulation, and treatment resistance remain incompletely validated in prostate cancer and are partly derived from studies in other malignancies. CCAT2 may eventually contribute to multimarker patient-stratification models if reproducible detection in prostate cancer tissue or biofluids is established. However, no standardized CCAT2 assay, independently validated clinical cutoff, prospective multicenter validation study, treatment-by-biomarker interaction analysis, or clinically evaluated CCAT2-directed therapy has yet been reported. This review critically distinguishes prostate cancer-specific findings from cross-cancer extrapolations, evaluates CCAT2 as an exploratory biomarker and experimental target-validation candidate, and defines the mechanistic, analytical, preclinical, and clinical studies required before its diagnostic, prognostic, predictive, or therapeutic utility can be established.