XIST (X Inactive Specific Transcript)

This study revealed a novel mechanism by which lncRNA-XIST promoted the malignant phenotype of glioma cells, which was found to be encapsulated inside apoptotic glioma cells rather than being released directly to the extracellular compartment. This finding revealed that it was possible to intervene in the function of lncRNA-XIST by inhibiting apoEV formation, thereby providing a new therapeutic avenue targeting lncRNA-XIST to modulate TMZ resistance in glioma.

We also include here a discussion of how these changes affect anti-cancer immunity and autoimmunity across a lifetime. These recent advances will set the stage for identifying immunotherapeutic approaches that optimize anti-cancer immunity while controlling the autoimmune responses.

All the data presented in the manuscript are supported by diverse experimental approaches, including transcriptional analyses, functional in vitro assays (migration, invasion, apoptosis), gain- and loss-of-function experiments, luciferase reporter assays, and in vivo xenograft models, further validating the miRNA-RKIP axis involved in the progression of multiple tumors. In conclusion, this review provides an integrated view of the complex post-transcriptional network governing RKIP regulation in cancer, underscoring the potential of targeting RKIP-associated non-coding RNA axes for innovative therapeutic strategies aimed at halting tumor progression and overcoming treatment resistance.

ORC1 represents a promising therapeutic target, as its inhibition induces replication stress, cell cycle arrest, and enhances sensitivity to existing chemotherapeutic agents. Future research should focus on developing specific ORC1 inhibitors and exploring their synergistic potential with immunotherapy and targeted therapies.

Our findings identify quercetin as a natural compound targeting the JPX-miR-495-3p-BRD4 cascade, providing both mechanistic insights and a translational rationale for quercetin-based NSCLC therapy. These findings highlight the therapeutic potential of quercetin in NSCLC and support further exploration of lncRNA-targeted strategies.

This review synthesizes emerging evidence on the role of lncRNAs in shaping nuclear architecture and gene regulation, with a focus on their oncogenic and tumor-suppressive functions. By integrating insights into chromatin topology and epigenetic control, we underscore the potential of targeting lncRNAs and associated chromatin remodeling pathways as innovative diagnostic and therapeutic strategies in cancer and other complex diseases.

Other lncRNAs aligned with oncogenic functions but lacked independent predictive value. Combining molecular and clinical parameters could improve risk stratification and early detection, warranting validation in larger cohorts.

In conclusion, our study elucidated new molecular mechanisms of nano-curcumin in the regulation of lncRNA expression and the discovery of potential targets in therapeutic interventions for CRC. More studies are needed to confirm the therapeutic implications of these findings.

Curcumin effectively inhibits EMT by inactivating the TGF-β1/Smads pathway through regulating XIST/miR-25-3p, and thereby alleviating the progression ofOSF. The study results further reveal the mechanisms underlying the function of curcumin, and may provide novel targets and ideas for OSF therapy.

In contrast, reduction of H3K9me3 caused partial reactivation of USP9X but not MED14, thus implicating a combinatorial action of silencing pathways in X-chromosome inactivation. Our work, in agreement with previous studies, reveals that in somatic cells XIST expression and localization suppresses the expression of escape genes.

Identification of canine XIST, previously annotated as LOC102156855, suggests a conserved mechanism of X-chromosome inactivation across species and a sex-specific epigenetic imprint on the genome, which is maintained independent of sex hormones. These findings enrich the understanding of sex-specific biology in dogs and highlight the intricate interplay between epigenetic modifications and gene expression in determining sex-specific phenotypes and disease susceptibilities.