MEG3 (Maternally Expressed 3)

This study indicates that XFC may upregulate the expression of lncRNA MEG3 and KLF4 by modulating METTL14-mediated m6A modification of lncRNA MEG3. Through this mechanism, XFC may regulate inflammatory responses and coagulation disorders, thereby improving SPP and exerting therapeutic effects on hyperinflammation-associated hypercoagulability in patients with OA.

Future research should prioritize paired tumor-node lncRNA profiling, validation of FNAB-based molecular assays, and integration of multi-omics data for predictive modeling. Overall, integrating lncRNA analysis into ultrasound-guided fine-needle aspiration biopsy may enhance the detection of occult nodal metastases in head and neck squamous cell carcinoma and support more accurate nodal staging in clinically node-negative patients.

The fact that alpha cells exhibit increased immune-like and anti-apoptotic activity as compared to beta cells suggests that they are better equipped to endure the autoimmune assault in T1D. In addition, the marked difference in the expression of the pro-apoptotic factor MEG3 in beta cells compared to alpha cells may explain, at least in part, why beta cells are more susceptible to damage and cell death in a diabetogenic environment than neighbor alpha cells within the same islet.

The quantitative evidence from numerous in vitro and in vivo studies has consistently demonstrated that flavonoid lncRNA modulation leads to a significant reduction in micro vessel density, expression of VEGF, and tumor burden. Improved bioavailability with more advanced nanoformulation and enhancement in preclinical validation of flavonoid lncRNA therapeutics, despite the remaining challenges like limited clinical data and off-target effects, offer low-toxicity targeted means of reprogramming tumor angiogenesis and overcoming resistance to the current therapies.

Elevated IL-6 and decreased NEAT1 define a peripheral signature linked to negative-symptom severity in SCZ and may support biologically informed stratification and longitudinal research.

The combination of cisplatin and metformin (Glucophage) exerts an additive cytotoxic effect and induces apoptosis in NSCLC cells in vitro. This effect is associated with a favorable modulation of key apoptosis-regulating genes and lncRNAs. These findings provide a strong rationale for further mechanistic and preclinical investigation of this combination therapy for lung cancer.

These results suggest that MEG3 knockdown impairs the anti-metastatic properties of DNC and OXA by modulating MMP-2 and MMP-9 expression. The combination of DNC and OXA holds promise as an effective therapeutic strategy in OC, and MEG3 may serve as a potential biomarker and therapeutic target, particularly in drug-resistant ovarian cancer.

These insights into lncRNA-mediated regulatory mechanisms provide promising therapeutic targets for RCC, suggesting that modulating specific lncRNAs or their associated pathways could offer innovative strategies for treatment and prognosis. This review presents a comprehensive analysis of the biogenesis, functions, and regulatory roles of lncRNAs in RCC, emphasizing their potential as diagnostic biomarkers and therapeutic targets to improve patient outcomes.

Our results demonstrated that MEG3 and its potential downstream regulator, F11R could be involved in PDAC progression, particularly in patients with long-DM. The findings underscore the clinical significance of epigenetic regulation in DM-related PDAC, suggesting novel targets such as MEG3 and F11R for potential therapeutic intervention.

Although challenges such as immune clearance, bacterial resistance, and regulatory complexity remain, the convergence of AI, CRISPR, and synthetic biology is accelerating the evolution of phage therapy into a clinically viable precision-oncology strategy. In this context, bacteriophages emerge not merely as antibacterial agents but as intelligent, patient-specific nanomedicines poised to redefine therapeutic boundaries in cancer treatment.

We further demonstrated that MEG3 expression is tightly controlled by the METTL3-YTHDC1 axis, and YTHDC1-mediated recognition of m6A-modified MEG3 is essential for the progression of RILI. These insights establish the YTHDC1-MEG3 pathway as a key molecular driver of RILI and provide a framework for the design of targeted therapies to mitigate RILI.