HMGB2 (High Mobility Group Box 2)

These effects were observed not only in KHYG-1 cells but also in NK cells derived from adult patients with head and neck squamous cell carcinoma. Our findings suggest that quinovic acid enhances NK cell cytotoxicity, showing promise as a potential therapeutic against various cancer cell types.

These results indicate that HMGB2 inhibits NK cell-mediated anti-tumor immunity in ESCC. HMGB2 depletion enhances NK cell cytotoxicity via the ANGPT1/PI3K/AKT pathway, suggesting its potential as a therapeutic target to improve NK cell-based immunotherapy in ESCC.

In summary, HMGB2+Epi represents a key lactylation-enriched subgroup, with the NFYB-HMGB2 axis driving CRC progression via lactylation. BI-2536 as a tool compound implicating the HMGB2-lactylation axis, and the HMGB2+Epi-based risk model provides a novel target for precision CRC therapy.

These findings unveil potential mechanistic pathways of comorbidity between HCC and HF, providing novel biological markers and therapeutic targets for the prognostic evaluation and treatment of these conditions, with substantial implications for refining clinical diagnosis and therapeutic strategies.

Integration with TCR-seq further uncovered immune microenvironment alterations and potential relapse biomarkers. These results demonstrate that combining deep learning with single-cell multi-omics is a powerful strategy for elucidating disease mechanisms, improving early diagnosis, and informing personalized therapies for pediatric ALL.

This study highlights the prognostic value of EC-derived immune genes in PCa and establishes a reliable gene signature model for PCa risk stratification. Notably, OPRK1 may serve as a novel therapeutic target, offering new insights into precision oncology and improving outcome prediction for patients with PCa.

Taken together, these findings highlight that HMGB2 plays a crucial role in promoting heart regeneration through regulating glycolysis. Activating the HMGB2-MTA2-HIF-1α axis might serve as a potential therapeutic option for regenerative therapies post-myocardial injury.

In addition, the prognostic signature retained independent predictive value for HCC RFS, and it was validated successfully by another publicly available dataset and RT-qPCR experiments using patient tissues. In conclusion, the present study constructed a prognostic model for predicting RFS in patients with HCC via integrated analysis of scRNA-seq and bulk RNA-seq data that could serve as a valuable reference tool for clinicians.

Genetic disruption of HMGB2 showed that it regulates the trade-off between proliferative and invasive states, in which confined HMGB2high tumour cells are less proliferative but more drug-resistant. Our results implicate the mechanical microenvironment as a mechanism that drives phenotype switching in melanoma.

HMGB2 knockdown experiments revealed that HMGB2 modulates migration and invasion of CC cell lines. In conclusion, the results of the present study suggest that miR‑124‑3p and miR‑23b‑3p modulate processes associated with carcinogenesis and tumor progression through their individual and shared target mRNAs and that the miR‑23b‑3p/HMGB2 axis is among the mechanisms that modulate migration and invasion in CC.

Both sets showed a promising clinical prediction value. In sum, this study preliminarily revealed the landscape of the TME in HR-NB at a single-cell level; several TME cell clusters that could inhibit immune activities or promote tumor progression in HR-NB were determined, thereby providing novel immunotherapeutic targets and an immune-related prognostic signature for HR-NB and promoting the development of immunotherapy of HR-NB.