CYTOR (Cytoskeleton Regulator RNA)

Furthermore, Western blot analysis revealed that silencing CD168 decreased the phosphorylation levels of ERK and MEK, suggesting that CD168 promotes LUAD progression in association with MAPK/ERK signaling pathway activity. In summary, CD168 may promote LUAD progression by reshaping the immunosuppressive microenvironment and enhancing malignant behavior, establishing it as a prognostic biomarker and a potential therapeutic target, particularly for immunotherapy combinations.

It was also determined that CYTOR suppression caused a decrease in the expression of the YAP1 gene, a key effector of the Hippo signaling pathway and the CTGF gene, one of its target genes. In conclusion, our findings suggest that CYTOR may be a potential therapeutic target in breast cancer by regulating the Hippo signaling pathway.

Panobinostat, Pirinixic acid, and Fluorouracil were predicted to be the potential BCL2L12-targeted drug for HCC. Our findings offer an understanding of the Oncogenic Role of BCL2L12 associated with immune status in the prognosis of HCC and provide potential strategies for currently limited treatment.

Through interactions with miRNAs and signaling pathways, these ncRNAs not only influence prognosis but also represent novel therapeutic targets. Integrating multiomics approaches and developing ncRNA-based biomarker panels are essential for advancing precision medicine in GC.

Our findings suggest that NanoCurcumin mitigates tamoxifen resistance by downregulating MALAT1, offering a novel epigenetic strategy to enhance endocrine therapy efficacy. Further studies should explore lncRNA-targeted interventions to improve treatment outcomes in ER+ breast cancer.

Furthermore, lncRNAs are implicated in DNA damage and genomic instability induced by H. pylori, as well as in creating the tumor microenvironment by regulating angiogenesis and immune evasion. This multifaceted involvement positions lncRNAs as promising diagnostic, prognostic, and therapeutic markers for H. pylori-associated GC, warranting further investigation for novel clinical interventions.

LINC00152 knockdown upregulates miR-103a-3p to reduce ADORA3 expression, thus protecting against the malignant biological behaviors and EMT of BLCA cells. The online version contains supplementary material available at 10.1007/s10616-025-00829-0.

Antisense oligonucleotides, small molecule inhibitors, and RNA interference are some of the strategies currently being investigated to dislodge the interactions between lncRNAs and histone-modifying enzymes, and they represent novel strategies for cancer therapy. This review summarizes recent advances in understanding lncRNA-histone modification crosstalk and its translation to the clinic for precision oncotherapy.

This study elucidates significant alteration in the cellular ecosystems and intercellular signaling within the tumor immune microenvironment across the NAT-HGIN-GBC sequence. It identifies TOP2A, TWEAK, and FN14 as potential biomarkers and therapeutic targets for GBC.

Experiments conducted both in vitro and in vivo revealed that CYTOR markedly stimulated melanoma cell proliferation, migration, and invasion. Dual-luciferase reporter assays confirmed the direct binding of miR-485-5p to CYTOR, and glucose-6-phosphate isomerase (GPI) was identified as a direct target of miR-485-5p.

This study, therefore, highlights the potential of identifying functional domains in noncoding RNAs. Delivery, or targeting of RNA domains might constitute next-generation RNA therapeutics.

CAF-derived exosomes harboring linc00152 enhance malignancy in cholangiocarcinoma, identifying a novel role of exosomal linc00152 for intensifying the crosstalk between CAFs and cholangiocarcinoma cells.