ITGA3 (Integrin Subunit Alpha 3)

In keratinocytes, BMRGs such as integrins (ITGB1, ITGA3, ITGA6), laminins (LAMA3, LAMC1), CD44, and FN1 were upregulated in cSCC compared to AK or BD (adjusted p < 0.05); in fibroblasts, BMRGs including ITGB1, ITGAV, LUM, BGN, SDC1, and FN1 were upregulated in cSCC (adjusted p < 0.05), suggesting their collective role in BM breaching and invasion, as well as a higher risk of BD. This study provides novel biological insights into the differentiation of progression pathways from AK or BD to cSCC, as well as potential targets for therapeutic intervention.

Notably, suppression of CACNA1C induced transdifferentiation from stable/late-state cells to normal epithelium-like cells. This study provides novel insights into the EMT mechanism in ESCC, proposes an intervention strategy, and emphasizes the promising clinical application of pathological images in EMT assessment.

In HNSC, the high expression of ITGA3/5/6 serves as a biomarker for poor prognosis. Our research results indicate that ITGA family genes can serve as valuable prognostic biomarkers and therapeutic targets for tumors.

This validated ARG-based prognostic model effectively predicts survival outcomes and revealed strong associations between anoikis resistance, immune landscape alterations, and immunotherapy response, offering a framework for risk stratification and precision immunotherapy in LUSC clinical management.

NNK is associated with a malignant transcriptional program characterized by epithelial remodeling, stromal interaction, and immune suppression. These molecular features can be captured non-invasively through CT-based radiomics. The NNK-related ITGA3-associated radiomics (NIR) score provides a practical tool for preoperative risk stratification in PC and offers a bridge linking environmental carcinogen exposure with tumor imaging phenotypes.

A 2E7-MMAE (monomethyl auristatin E) ADC exhibited potent, dose-dependent antitumor activity in bladder cancer xenograft models, leading to tumor regression and prolonging survival. This study establishes a generalizable framework for function-first ADC discovery and nominates ITGA3B1 as a promising therapeutic target in bladder cancer.

Our findings indicate that epithelial cells undergo profound changes during lung cancer brain metastasis. ARGs, particularly CD44, play a critical role in this process and have prognostic significance for lung cancer brain metastasis.

Baseline EMT/adhesion signatures and stress-response pathways nominate CD44 and ITGA3/α3β1 as candidate biomarkers of resistance. These findings delineate molecular programs of β-emitter radioresistance and identify candidate pathways for future targeting.

Kyoto Encyclopedia of Genes and Genomes and Gene Ontology enrichment analyses showed that QsCATH balanced inflammatory resolution with host defense by modulating biological processes including "immune system processes," "defense responses," and "oxidative stress responses." Using molecular docking simulations, potential interactions were predicted between QsCATH and membrane-associated proteins Nod2, Ripk2, and Itga3 (binding scores: - 239.00, - 213.24, and - 290.08, respectively), suggesting direct interference with receptor-mediated signaling cascades. This study presents the first transcriptome-level analysis of the immunoregulatory network of amphibian cathelicidins, providing insights for developing novel peptide-based therapeutics against drug-resistant infections and inflammatory disorders.

ITGA3 expression in tumor tissue significantly aids in predicting LM in EOC patients and is independently and closely related to adverse clinicopathological outcomes.

These findings suggest that Siglec-10 interactions are key mediators of TAM-driven immune evasion in PDAC and highlight the therapeutic potential of targeting these interactions to restore antitumor immunity. Pancreatic tumor cells exploit integrin α3β1 to engage the immunosuppressive checkpoint receptor Siglec-10 on myeloid cells, driving immune evasion, which can be targeted with antibody-mediated blockade of Siglec-10 to restore antitumor immunity.