STAT3 (Signal Transducer And Activator Of Transcription 3)

Raman spectroscopy revealed that lipid spatial localization correlated with RNA expression in the spleen and lymph nodes, highlighting the importance of LNP structure in immune activation and targeting specific immune organs. Functionally, A3-DM/DL-LNPs restored dendritic cell (DC) antigen presentation, alleviated endoplasmic reticulum (ER) stress, and reversed T cell exhaustion in acute myeloid leukemia (AML), triggering strong immune responses and enhancing natural killer (NK) cell and T cell-mediated antileukemic activity, thereby improving therapeutic outcomes.

The findings suggest that phytochemicals can modulate multiple checkpoints with a favorable safety profile. Future research must focus on rigorous clinical trials to establish standardized dosing and validate safety margins for translating these agents into effective personalized melanoma immunotherapies.

More importantly, the ATO from ATO/CR NPs can also specifically target STAT3 in GC cells to restrain proliferation, inhibit angiogenesis, and promote apoptosis. Hence, the multimodal NIR ATO/CR NPs initiate accurate targeting of cancer cells, triggering serious mitochondrial dysfunction and cellular apoptosis to amplify the photo-ablation activity, which provides a promising strategy for GC treatment, warranting further preclinical exploration.

Current multi-omics analysis delineates STAT3 and HIF1A as central regulators coordinating apoptotic and necroptotic cross talk in LUSC. Deleterious nsSNPs within these TFs highlight structural vulnerabilities potentially driving tumor progression and therapeutic resistance, offering promising targets for precision-based intervention.

Advances in engineering, such as Angiopep-2-functionalized exosomes for blood-brain barrier penetration and CRISPR-Cas9-loaded vesicles targeting resistance genes, highlight their therapeutic potential. Challenges in heterogeneity, standardization, and scalable production underscore the need for interdisciplinary innovation to translate exosome-based strategies into clinical practice.

It also highlights emerging therapeutic approaches, such as antisense oligonucleotides, RNA interference, CRISPR-Cas systems, and natural lncRNA-modulating compounds, which collectively represent a promising frontier in precision medicine for brain tumors. This work offers a critical framework for future research and therapeutic innovation in the lncRNA landscape of neuro-oncology.

Six compounds were isolated from H. giganteus, with 4 exhibiting antiproliferative activity through PRKCA and GSK3β modulation. These findings provide the first phytochemical and mechanistic evidence that support H. giganteus as a promising source of active anti-colon cancer leads.

This review provides a comprehensive synthesis of the sources, pharmacological actions, safety, pharmacokinetics, and potential applications of GS. Future research should focus on structural modification of GS, development of novel formulations, and exploration of synergistic combinations with other therapeutic agents to broaden its clinical utility.

In vivo, xenograft models further validated that BUB1 silencing significantly reduces tumor volume, accompanied by modulation of ferroptosis-related genes in tumor tissues. Collectively, our findings identify BUB1 as a novel prognostic biomarker and therapeutic target for LUAD, revealing a new regulatory mechanism by which BUB1 promotes LUAD progression through the activation of the STAT3/GPX4 axis to suppress ferroptosis.

KT-333 significantly decreases STAT3 and MCL1 protein levels and improves survival in Ven-resistant (Ven-Res) AML murine models. Pictorial representation depicting upregulation of STAT3 and MCL1 in venetoclax resistant myeloid malignancies such as MDS and AML causing mitochondrial structural abnormalities and dysfunction. By using specific STAT3 degrader, STAT3 inhibition, and thereby indirect downregulation of MCL1 can be a promising therapeutic intervention to target drug resistant clones in MDS and AML.

DNMT3A and METTL7A were shown to cooperatively regulate DDR1 via DNA/m6A methylation, which drives Treg-mediated immune suppression and recurrence. This study provided novel insights and therapeutic targets for breast cancer prognosis and treatment.