ITGB1 (Integrin Subunit Beta 1)

In OC mice, TRIM28 overexpression promotes angiogenesis and Bev resistance via ESM1-mediated ITGB1/FAK activation. This work unveils a new molecular pathway underlying Bev resistance in OC and proposes TRIM28 and ESM1 as potential therapeutic targets.

These findings position tumoral ITGB1 as a promising therapeutic target for reprogramming the TME from a pro- to an anti-tumorigenic state, thereby effectively inhibiting TNBC development. Our study uncovers a novel mechanism of TNBC development and provides a unique therapeutic strategy for targeting ITGB1 in TNBC treatment.

Our findings indicate that SE-driven TCF4 can orchestrate metastatic transcriptional networks to maintain NB malignancy and propose ACY-1215 as a translational therapeutic candidate for clinical intervention.

This study comprehensively characterized the molecular features of BCSCs through multi-omics approaches, identified reliable surface markers and key regulatory genes, and constructed a prognostic prediction model with clinical application value.

Products of these genes are renowned drivers of tumor progression. We have developed a software algorithm for the design of unmodified and modified siRNAs, carried out solid-phase synthesis of the most promising molecules, and proved their capability to perform a more than 50-fold suppression of expression of the target genes in vitro.

Despite the small sample size and absence of functional experiments, our results suggest that Pazopanib promotes cytotoxic immune programs but, by six months, reprograms PLT-EVs towards different adhesion characteristics contributing to Treg and MDSC expansion while suppressing NK activity. PLT-EVs may influence the balance between immune activation and suppression during anti-angiogenic therapy, suggesting PLT-EVs as biomarkers and therapeutic targets in mRCC.

Furthermore, risk models incorporating specific protein signatures effectively stratified patients by platinum sensitivity/resistance (9-protein panel: ILK, CDCP1, CD86, CLDN4, CLEC1B, CDHR5, CLDN11, JAM2, FOLH1), lymph node metastasis status (7-protein panel: APOE, CD28, CLDN4, FOLH1, ITGAL, JAML, ULBP3), and post-surgical residual disease burden (4-protein panel: CD44, CLMP, ITGA4, AMIGO1), with Cluster 13 (ITGB1-high) also significantly associated with residual disease. This work demonstrates the power of single-EV proteomics combined with machine learning for non-invasive diagnosis and clinical outcome assessment in advanced ovarian cancer, though the absence of early-stage patients limits its applicability for early detection.

Leveraging cell-type-specific genes and key ligand-receptor pairs, we developed a Mucinous Colorectal cancer Immune Module (MCIM) comprising 18 genes, which stratified patient prognosis and was associated with overall survival in colorectal cancer cohorts. Together, these findings provide a detailed map of the immune-stromal architecture in MAC with MSS status, reveal macrophage-associated immunosuppressive features, and propose MCIM as a potential biomarker for prognostication in mucinous colorectal cancer.

An 18-month HFD successfully established a translational M. fascicularis model replicating key metabolic disorders (MASH, diabetes, cardiac hypertrophy). BAAT, CS/MDH1/H6PD, and SRC/MAPK14/EMD/ITGB1 were identified as mechanistic biomarkers for these conditions.

Our findings demonstrate that EV composition remains stable in Protein Plus BCT compared to EDTA and ACD-A tubes, with a small number of exceptions. This insight into EV stability in blood specimens is crucial for advancing EV biomarker research in neurological disorders, including Alzheimer's disease, potentially enhancing diagnostic accuracy and therapeutic strategies.

Our study establishes FF-fibronectin as an important regulator of the early peritoneal seeding of HGSC precursor cells. These findings reveal a direct link between ovulation and HGSC development, suggesting that targeting the FN-ITGB1 signaling axis may offer a novel preventive strategy for high-risk individuals.

We find that lineage transition is accompanied by a redistribution of FOXA1 and TEAD cistromes from PRAD to NEPC-specific enhancers and requires the pioneering activity of FOXA1. Thus, extracellular matrix/integrin signaling in the PRAD tumor microenvironment restrains NE lineage plasticity, highlighting a potential path for pharmacological inhibitors in modulating treatment-induced lineage change.