ITGB5 (Integrin Subunit Beta 5)

This loop was augmented in CRC specimens from patients with distant metastasis. Our study elucidates a novel RBP-integrin regulatory axis in CRC metastasis and proposes the STAU1-ITGB5-FOXP3 loop as a prognostic biomarker and promising therapeutic target for metastatic CRC.

Collagen fiber density/alignment and MYC/AP-1 gene signatures served as pharmacodynamic readouts of drug activity. These data uncover a tractable ECM-integrin-MYC axis in ILC and nominate PXS-5505, alone or with endocrine therapy, for window of opportunity trials in this understudied breast cancer subtype.

The reduced tumorigenic behavior of glioblastoma cells due to HOXA10-AS knockdown can be rescued by ITGB5 overexpression or miR-99a-3p inhibitor. These results indicate that HOXA10-AS promotes tumorigenic behavior in glioblastoma cells by regulating the EMT-like process and functioning as an miR-99a-3p sponge to modulate ITGB5 levels, providing insights into glioblastoma development and potential therapeutic targets.

POSTN+ fibroblasts may interact with MSLN+ budding-potential cells through the ligand-receptor pair POSTN-ITGB5 to promote tumor metastasis. In conclusion, our findings identified the transcriptomic feature of budding-potential cells and revealed the role of crosstalk between MSLN+ budding-potential cells and POSTN+ fibroblasts in CRC metastasis, which provide new insights into targeting cancer-associated fibroblasts and tumor budding cells in CRC therapy.

Specifically, CAFs exhibited significantly higher expression levels of COL7A1 compared to normal pancreatic fibroblasts, and COL7A1 knockdown in CAFs markedly reduced the migratory capacity of PC cells while enhancing their chemosensitivity to gemcitabine...This model, incorporating pivotal genes of PCLM and BM, may also serve as potential tool for predicting the tumor immune microenvironment and therapeutic efficacy. Notably, COL7A1, which was demonstrated to be vital in PC metastasis in this study, warrants further investigation in future research.

Our findings highlight the critical role of COL6A3+ TAFs in regulating MDM function and spatial distribution, as well as their contribution to fibrotic tumor vasculature formation. Additionally, we propose targeting COL6A3+ TAFs with cilengitide as a potential therapeutic strategy.

The integration of magnetic resonance elastography, atomic force microscopy, and single-cell sequencing allows detailed research characterization of the biomechanical properties of PDAC. ITGB5 has been identified as an important regulator of the biomechanical features of PDAC. Targeting ITGB5 in CAFs may reduce the excessive stiffness of PDAC tissue and mitigate gemcitabine-associated stromal fibrosis, suggesting a potential strategy to improve treatment response. The effect on patient prognosis, however, requires confirmation in clinical studies.

ΔC499 induces M2 macrophage polarization and drives PCa invasiveness by modulating ITGB5, TIMP1, and TMEM176B. Three genes signature is differentially expressed between aggressive and indolent tumors, providing potential non-invasive biomarkers to discriminate aggressive from indolent PCa.

Machine learning refined a 4-gene prognostic signature (CLN6, GMPR, AP1S2, ITGA6), with functional validation confirming the role of CLN6 in proliferation and migration. This study establishes a prognostic framework and therapeutic roadmap for precision immuno-oncology in melanoma, bridging multi-omics discovery with clinical translation.

Our findings suggest that ncRNA-mediated ITGB1 expression is associated with poor prognosis and tumor-immune infiltration in GC. However, further validation through extensive mechanistic studies and large-scale clinical trials is warranted.

Pharmacological inhibition of the POSTN-integrin axis partially reversed these malignant traits, highlighting its potential as a therapeutic target. This study provides new insights into fibroblast heterogeneity and its role in PDAC progression, emphasizing the POSTN-ITGAV/ITGB5 axis as a promising target for therapeutic interventions.

Therefore, we introduce regulatory cascades as novel initiating and key events within the Adverse Outcome Pathway (AOP) framework, revealing for the first time the precise mechanisms underlying the inflammation-to-cancer transition driven by Cd-MP co-exposure. Our study aligns with the FDA's newly announced alternative approaches to toxicology, demonstrating how the integration of computational and experimental methods can enhance regulatory frameworks for assessing complex pollutant exposures.