CRNDE (Colorectal Neoplasia Differentially Expressed)

Mechanistically, Crnde modulates the mRNA expression of gastrulation brain homeobox 2 (Gbx2), a gene critical for thalamic development. Collectively, our results implicate lncRNA Crnde in the proper progression of embryonic thalamic development in mice.

Our analysis of specific lncRNAs, such as HOTAIRM1, HOXB-AS3, CRNDE, HOXBLINC, LONA, IFEX9, XLOC_109948, and HOTTIP, enhances our understanding of the molecular mechanisms underlying AML in the context of NPM1c⁺. These findings lay the groundwork for developing targeted therapies and improved prognostic tools for NPM1c⁺AML.

Although current research remains exploratory, lncRNAs show significant promise as predictive biomarkers and therapeutic targets. Future personalized strategies intergrating lncRNA profiles could help overcome drug resistance and improve patient outcomes.

Ependymal YAP signaling promotes the formation of ependymal cell-derived perilesional glial borders in mice through the P300-CRNDE-Wnt/β-catenin pathway after SCI, which provides a novel target for SCI.

Subsequently, the role of TRA2B in the tumor immune microenvironment (TIME) was investigated. In summary, this research provides novel insight into the potential role of TRA2B across various cancers and indicated that ncRNA-mediated overexpression of TRA2B is associated with the dismal prognosis in HCC.

eRNAs are not passive transcriptional by-products but active modulators of glioma biology. They influence tumor initiation, therapeutic resistance, and survival outcomes, underscoring their potential as prognostic biomarkers and therapeutic targets. Future research should validate these findings in larger clinical cohorts and explore strategies for eRNA-directed therapies in precision neuro-oncology.

In a rat model of rotator cuff tear (RCT), transplantation of CRNDE-overexpressing TDSCs significantly enhanced functional recovery, an effect associated with upregulation of TGFBR2. Taken together, these results demonstrate that CRNDE promotes tenogenic differentiation and tendon-bone healing through modulation of the miR-337/TGFBR2 signaling axis.

By underscoring the reversibility of epigenetic changes, we explore their translational potential in early detection, surveillance, and precision epigenetic therapy. Understanding the interplay between genetic mutations and chromatin remodeling provides a roadmap for improving diagnostics and personalized treatments in inflammatory bowel disease-associated colorectal carcinogenesis.

While the study offers significant contributions to the field, there are limitations in its methodology, interpretative depth, and generalizability that merit closer examination. This commentary critically evaluates the findings, suggesting avenues for refinement and further research.

We further show that CRNDE exerts downstream effects on MM cell survival, tumorigenic potential, and stem-like properties via an effect on the SIRT1/Hh signalling axis. Our findings add to the molecular understanding of the pro-tumorigenic activity of CRNDE in MM and could have wider implications in other malignant diseases.

Notably, the overall expression of genes identified in Stage 4 could significantly differentiate patients' survival outcomes. Moreover, the genes we identified could distinguish patients' responses to immunotherapy.

In summary, we obtained 5 lncRNAs that may be closely related to colorectal cancer, including NCAL1, CRNDE, HMGA1P4, EPIST and MT1JP. This study found that NCAL1, HMGA1P4, EPIST and MT1JP may be candidate biomarkers for colorectal cancer.