ITGA6 (Integrin, alpha 6)

We unveiled a novel, EV-derived protein signature that has potential to be further applied for future functional studies, non-invasive diagnostic assays and targeted therapeutic interventions against BlCa.

Notably, these findings were recapitulated through pharmacological inhibition of FAK signaling using Defactinib, an FAK-specific inhibitor. Taken together, our findings reveal that bone-marrow ssDNA may represent a bone microenvironment factor that captures and promotes PCa homing to bone, further suggesting a potential therapeutic strategy for mitigating bone metastasis.

Transcriptomic profiling combined with machine learning provides a promising approach for predicting NAC response in TNBC. The identified biomarkers may inform precision treatment strategies and improve clinical outcomes in this high-risk patient population.

INHBA/ITGA6/MAPK axis can provide new insights into GC therapy. Targeted INHBA inhibition holds promise as a therapeutic approach for GC treatment.

ASH2L promotes tamoxifen resistance and CSC activity through ITGA6/ERK signalling. Combination therapy with tamoxifen and an ERK inhibitor may be a promising strategy for ER-positive breast cancer patients with ASH2L overexpression.

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.

Disruption of LAMA4-ITGA6 binding substantially attenuated FOXC2-LAMA4-mediated metastatic burden. These results reveal a novel mechanism by which FOXC2+ tumor cells promote metastasis in advanced ccRCC and further establish the therapeutic potential of targeting FOXC2-LAMA4 in blocking the metastatic cascade of ccRCC.

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.

Finally, hMSCs expanded on S75H25 were successfully differentiated into adipogenic, chondrogenic, and osteogenic cell types. We engineered chemically defined and highly economical GAG-mimetic cell culture substrates based on sulfonated polymer brushes that can be readily applied to biomanufacturing platforms such as spinner flasks, bioreactor beads, and microfluidic platforms to boost hMSC throughput under fully defined conditions.

CD97, CD73, CD86, and CD58 are the best amongst newer markers in B-ALL MRD assessment. Our findings support integrating these into MRD panels to enhance post-therapy MRD detection, thus improving prognostication and guiding treatment decisions.

We found that csPCNA is co-expressed with CD44, CD49f, PD-L1, and TGFβRII on the primary patient-derived GBM specimen. Our findings that csPCNA is expressed in GBM and is co-expressed with stem cell and immunosuppressive biomarkers indicate that csPCNA may be a potentially useful clinical-pathological biomarker for GBM stemness and immunosuppression.

Based on our results, the CD49f molecule can be used as a measurable residual disease marker in both pediatric and adult B-cell acute lymphoblastic leukemia patient groups, and its expression correlates with genetic abnormalities and focal adhesion kinase-Src pathway activation. Orv Hetil. 2025; 166(50): 1983-1992.