IRAK1 (Interleukin 1 Receptor Associated Kinase 1)

Importantly, PTPN22 knockout abrogated the anti-migratory effects of IRAK-M, confirming its essential role in this pathway. These findings establish the IRAK-M-PTPN22 axis as a critical suppressor of melanoma metastasis within the tumor microenvironment and highlight its potential as a therapeutic target to limit tumor dissemination and improve patient outcomes.

Notably, silencing RPS28 also disrupted both the oncogenic phenotype and downregulated MTA1, IRAK1, and TMSB10 expression. These findings reveal a complex interplay between FBL, rRNA Nm modifications, and RPS28 in shaping oncogenic protein pools and ribosomal composition in TNBC, offering promising insights into therapeutic approaches targeting this aggressive cancer subtype.

These integrated molecular effects were superior to those of free apigenin or blank EVs. Collectively, our findings highlight Apig-exo as a potent, multi-modal therapeutic platform capable of overcoming TNBC resistance via coordinated modulation of microRNA networks, apoptotic pathways, and epigenetic landscapes.

These findings establish SLC10A3 as a promising therapeutic target in HNC. Its consistent upregulation, association with poor prognosis, and potential interactions with key regulatory proteins highlight its relevance for future therapeutic strategies.

MiR-146a prevents AAA formation and progression by maintaining VSMC homeostasis in the proinflammatory microenvironment. Upregulation of miR-146a in the aortas shows great potential as a new therapeutic strategy to limit AAA expansion and progression.

STRING analysis identified IKBKB as a central hub in the PPI network, while GO enrichment highlighted immune regulation, apoptosis, and NF-κB signaling. These findings demonstrate that adalimumab modulates NF-κB activity in keratinocytes through coordinated regulation of gene, protein, and miRNA expression, providing mechanistic insight into TNF-α blockade in psoriasis.

These results indicate dual roles of in situ induced HSP70 in antigen delivery and immunoregulation at physiological conditions. These dual functions highlight opportunities to exploit endogenous HSP70 for both vaccine adjuvantation and immunomodulation.

Adverse events, including gastrointestinal symptoms, weight loss, and transient voice changes, were manageable through dose adjustments and supportive care, enabling continued therapy. Our cases contribute to the growing body of evidence supporting pacritinib's role in the evolving treatment landscape of MF.

Notably, we found that gastric cancer cells display marked sensitivity to IRAK1/4 inhibitor and pacritinib, the latter targeting JAK2 and IRAK1 specifically, over the pan-JAK inhibitor tofacitinib. Collectively, our results underscore IRAK1 as a promising therapeutic target in gastric cancer. Furthermore, the pharmacological blockade of IRAK1 by pacritinib, an established drug for myelofibrosis and severe thrombocytopenia treatment, holds potential for repurposing in gastric cancer therapy.

Nonetheless, HTP therapy alleviated hepatic damage via regulating redox profile, inflammatory and apoptotic indices, and histopathological alterations. Our findings were strengthened by computational analysis that revealed the strong binding affinity of HTP with key regulatory genes thereby showing its pivotal role in regulating gene expressions.

IRAK inhibitors and degraders are promising treatments for a variety of cancers. Future clinical success will depend on optimizing kinase selectivity profiles and identifying biomarkers to guide patient selection and combination strategies.

These findings demonstrate that miR-146a-enriched EVs effectively modulate immune responses, suppress neuroinflammation, and promote neuroprotection in EAE, highlighting their potential as a novel therapeutic strategy for MS. By targeting both inflammatory and degenerative pathways, miR-146a-enriched EVs represent a multifaceted approach to address the unmet needs in MS treatment.