MMP3 (Matrix metallopeptidase 3)

Furthermore, the clinical trial indicated that our nanosensor could noninvasively, conveniently, and effectively distinguish healthy individuals from oral cancer patients, and those with lymph node metastasis. This strategy offers a robust framework for multi-marker detection in clinical diagnostics, facilitating high-frequency and large-scale cancer screening through saliva test.

We identified seven genes that are persistently upregulated during the progression from HC to UC and CAC. These genes influence neutrophils and inflammatory/tumorigenic pathways. The upregulation of PD-L1 in neutrophils suggests that neutrophil-mediated immune suppression may contribute to CAC progression, supporting their potential as molecular markers and therapeutic targets for early intervention in UC-related cancer.

Elevated mRNA levels of EMP3, THBS2, and ITGA5 were significantly correlated with poorer overall survival. Fn and Pg can promote invasive phenotypes in CRC through distinct mechanisms, each modulating a unique subset of p-EMT and without instigating a complete, coordinated EMT gene signature.

In patients with axSpA, TNFi therapy significantly reduces serum VEGF levels and effectively reduces disease activity. VEGF has the potential to function as a dynamic biomarker that reflects the characteristics of the disease and the response to treatment.

These findings highlight the potential of GDEVs as an anti-inflammatory therapy for RA. Given their stability and bioavailability, the oral administration of GDEVs could be a promising non-invasive treatment for future clinical applications.

Furthermore, we discuss emerging therapeutic strategies for KMT2C-deficient breast cancers, such as epigenetic modulators (EZH2 inhibitors, KDM6A inhibitors, and BET inhibitors), DNA damage response (DDR)-targeting agents, and pathway-specific inhibitors. These insights not only elucidate the complex biological functions of KMT2C in breast cancer but also provide a rationale for developing precision therapies tailored to KMT2C-mutant tumours.

The results of this research provide value to the field of proteomics as a large-scale, reproducible, and hypothesis-generating plasma dual-omics reference dataset. This study was not designed to establish diagnostic biomarkers, to assess clinical discriminative performance, or to imply causal mechanisms. Instead, by emphasizing reproduciblilty across independent cohorts, we provide a plasma dual-omics reference dataset that captures coordinated immune and lipid metabolic alterations associated with chronic liver disease severity. These data provide a framework and resource for future studies researching risk stratification, therapeutic monitoring, and mechanistic validation in chronic liver disease.

LIFI demonstrated strong discrimination (C statistic, 0.83) and was associated with post-LT infections, longer hospital stays, and reduced patient survival. Per the results of this diagnostic/prognostic study, LIFI identifies LT candidates with severe immune dysfunction at high risk for early post-LT mortality, offering a preoperative, objective tool to refine transplant candidacy, guide perioperative management, and improve LT outcomes.

Furthermore, curcumin significantly inhibited tumor growth (p=0.039) and exhibited a synergistic antitumor effect with oxaliplatin in vivo. This study comprehensively elucidates the molecular mechanisms by which curcumin exerts its therapeutic effects in CRC via modulation of ferroptosis and Wnt/β-catenin signaling pathway. These findings provide novel mechanistic insights and support the translational potential of curcumin in preclinical and clinical frameworks.

Our findings demonstrate that ELOVL3 correlates with cancer cell stemness and angiogenic potential, thereby identifying it as a promising therapeutic target. Further investigations are warranted to elucidate the downstream molecular pathways that mediate these functional effects.

In vitro, CCNB1 knockdown triggered cell cycle arrest, thereby suppressing the proliferation of colorectal cancer cells. This study validated CCNB1 as a dual-purpose biomarker for CRC diagnosis and favorable prognosis, highlighting its potential utility in clinical management.

These findings suggest that MMP3 engineering is a simple yet effective strategy to overcome stromal barriers and enhance the efficacy of CAR-T cell therapy in solid tumors.