MIR22 (MicroRNA 22)

In conclusion, our combinational sequencing approach unraveled several small non-coding RNAs with a significant post-transcriptional impact on BrCa cell signaling. The online version contains supplementary material available at 10.1007/s10142-026-01856-6.

Additionally, high WDHD1 levels were associated with increased CD4 memory T cell infiltration, elevated tumor mutational burden (TMB), and enhanced expression of key immune checkpoint markers, suggesting a potential for improved response to immunotherapy in these patients. These findings suggest WDHD1 as a novel oncogenic driver and promising therapeutic target in HCC.

In conclusion, circulating microRNAs, particularly miR-451a and let-7a-5p, show promise as supportive biomarkers that may complement existing diagnostic and risk assessment tools in MDS. Further studies are needed to validate their clinical applicability.

Emerging strategies to modulate NLRP3 include small-molecule inhibitors (e.g., MCC950, BAY-117082), plant-derived compounds (e.g., oridonin, Bacopa monnieri), and immunotherapy approaches, including intratumoral NLRP3 agonists combined with checkpoint blockade. This review synthesizes the multifaceted roles of NLRP3 in OSCC, highlighting its centrality in inflammation-driven tumor biology and its promise as a therapeutic target. Understanding the contextual duality of NLRP3 activation is critical for developing precision therapies that disrupt its tumor-supportive effects while preserving or enhancing its immunogenic functions.

These findings identify a previously unrecognized HuD-PPARα-FAO axis that restrains metabolic stress and senescence. By linking post-transcriptional regulation to lipid metabolism and inflammatory signaling, this work highlights stress-induced premature senescence as both an outcome and a propagator of metabolic dysfunction, providing insight into mechanisms of aging-related vulnerability.

Notable differences in miRNA expression profiles were revealed for the patients with brain metastases from lung cancer, suggesting the role of the selected miRNAs in cancer metastasis to the CNS. However, while our analysis provides exploratory insights, the findings should be interpreted with caution and require validation in larger, independent cohorts before any clinical or translational implications can be established.

Pathway and immune profiling analyses demonstrated convergence of canonical immune signaling pathways, including JAK-STAT and PI3K-Akt, with neuronal communication modules, accompanied by enhanced innate immune signatures. Although limited by reliance on public datasets and small sample size, these findings delineate a systems-level neuroimmune regulatory program in anti-NMDAR encephalitis and provide a scalable, network-based multi-omics framework for investigating immune-mediated neurological and autoimmune disorders and for guiding future experimental validation.

Through expression profiling, correlation assessment and survival evaluation, we identified that the FGD5-AS1/miR-22-3p axis was the most potent upstream non-coding RNA regulatory pathway for CD47 in HCC. Our findings systematically characterise the CD47-SIRPα axis as a negative prognostic indicator and an immunotherapeutic target in HCC.

Therefore, the NLRP3 inflammasome represents a key player in cancer development, and its regulation by miRNAs highlights its importance and clinical potential. This review summarizes mechanistic and clinical knowledge on the biology of NLRP3, highlights its dual role in cancer hallmarks, and discusses the therapeutic promise of targeting the NLRP3-miRNA axis in the management of oral cancer.

In summary, the miR-22-Gal-1 axis can be an HCC prognostic biomarker, and it has vital roles in regulating metabolism and tumor immunity.

These results suggest that miR-22 acts as a tumor suppressor in GBM and CD133+ GSCs. Therefore, miR-22 represents a potential therapeutic target for cancer stem cell-based glioblastoma treatment.