ZFAS1 (ZNFX1 Antisense RNA 1)

Lastly, ZFAS1 suppression decreased cell viability both at baseline and in response to acute thapsigargin treatment. This work identifies novel ZFAS1 variants and uncovers a link between ER stress and ZFAS1 through the UPR.

Clinically, plasma ZFAS1 demonstrates enhanced diagnostic utility when combined with alpha-fetoprotein (AUC = 0.891), while therapeutic targeting of ZFAS1-mediated PI3K-AKT and PERK/ATF4 pathways shows promise in overcoming sorafenib/donafenib resistance. Current translational challenges include ZFAS1 isoform heterogeneity, suboptimal liquid biopsy sensitivity, and dynamic TME interactions. Future directions should employ multi-omics integration (spatial transcriptomics/single-cell sequencing) coupled with AI-driven network modeling to systematically decode ZFAS1's regulatory architecture, ultimately enabling precision theranostic strategies for HCC management.

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 results highlight the pivotal role of ZFAS1 in gastric cancer cell malignancy, which inhibits the activation of the AKT/mTOR pathway. The regulatory involvement of SP1 in ZFAS1 transcription provides a novel understanding of the molecular mechanisms driving cancer progression and offers potential therapeutic avenues by suggesting that further research could focus on developing targeted therapies that modulate ZFAS1 expression or activity, which may lead to more effective treatment options for gastric cancer patients in the future.

Our study disclosed the diagnostic utility of plasma HOTIP, BANCR, ZFAS1, TINCR, GC1, and AFAP1-AS1 lncRNAs as appropriate diagnostic biomarkers for gastric cancer. The identification of dysregulated lncRNAs offers promising avenues for noninvasive diagnostic assessment in gastric cancer.

These findings demonstrate that the ZFAS1/STAT3 signaling axis contributes to imatinib resistance in CML through the modulation of glucose metabolism. Targeting this regulatory pathway may represent a novel therapeutic strategy to overcome TKI resistance in CML.

As a proof of principle, we studied the regulation of DICER1, a cancer gene that plays a key role in microRNA biogenesis, by the lncRNA ZFAS1. We showed that ZFAS1 helps activate DICER1 transcription and block its mRNA degradation to phenomimic DICER1 and regulate its target microRNAs.

By influencing the miR-1953/TAZ signaling pathway, ZFAS1 significantly contributes to the activation and EMT of HSCs in liver fibrosis development. These findings highlight ZFAS1 as a potential therapeutic target for treating liver fibrosis, offering new avenues for clinical intervention.

ZFAS1 promotes prostatitis to cancer transformation by activating the NF-κB signaling through promoting MYD88 dimerization and the subsequent myddosome assembly.

Overall, we provide evidence that m6A lncRNAs are strongly modulated in gliomas, representing biologically distinct subgroups. Ten novel differentially methylated lncRNAs were identified in gliomas, which might exert regulatory role in glioma cells. These findings may provide a basis for further deeper research on the role of m6A lncRNAs in gliomas.

As a result, the conclusions of this manuscript are considered substantially compromised. The authors have been informed about the retraction.

These studies reveal a novel feedforward lncRNA circuit contributing to pulmonary carcinogenesis and suggest that pharmacologic targeting of SP1 and/or NFĸB may be useful strategies for restoring ZNFX1 expression for lung tumor therapy.