BACKGROUND: JPX is a long non-coding RNA involved in X-chromosome inactivation through regulation of XIST. In cancer research, its reported role varies across tumor types and is often discussed in separate mechanistic axes. This review re-examines the current literature with emphasis on context dependence, the JPX-XIST relationship, evidence strength, and translational caution. METHODS: PubMed was searched up to November 2025 using combinations of "JPX" or "Jpx" with "lncRNA," "XIST," "cancer," "tumor," "carcinoma," and tumor-specific terms. Peer-reviewed studies that evaluated JPX expression, function, or clinical relevance in cancer were included. RESULTS: Available evidence indicates that JPX has context-dependent roles in human cancers. In lung cancer, esophageal squamous cell carcinoma, oral squamous cell carcinoma, osteosarcoma, cervical cancer, gastric cancer, ovarian cancer, glioblastoma, head and neck squamous cell carcinoma, and endometrial cancer, JPX has mainly been reported in oncogenic settings. Proposed ceRNA-like mechanisms were common in these tumors. In hepatocellular carcinoma, breast cancer, and uveal melanoma, the published findings were more consistent with XIST-related tumor-restraining programs. The evidence remains uneven. Many reported mechanisms came from single studies, limited model systems, or lacked independent validation. CONCLUSION: JPX should not be regarded as a uniformly oncogenic lncRNA. Its role appears to depend on tumor context, the dominant downstream program, and, in some settings, the status of the JPX-XIST axis. JPX is better viewed as a candidate biomarker and an experimental target than as a clinically validated one.
Li et al. (2026) studied this question.