CDH11 (Cadherin 11)

In the female-specific panel, genes related to aberrant androgen signaling across tumor types like AR, PLXNA1, USP54, and PMEPA1 were influential. These results offer potential targets for further in vivo/vitro experimentation and provide a framework for constructing generalizable, high-performance gene panels for bladder cancer diagnosis and prognosis.

Cdh11, but not Cdh2, in CAFs is important for collective migration. These findings highlight how differential cadherin-mediated communication between cells maintains organization during collective migration.

These results suggest that CDH11 is involved in BC progression and is a potential therapeutic target.

As the mechanism, FOXP3 induced CDH11 expression in fibroblasts, which augmented the Wnt3/β-catenin pathway, and blocking of CDH11 suppressed tumor invasion mediated by FOXP3(+) fibroblasts. Our results suggest that cancer cell-derived EVs regulate FOXP3 expression in stromal fibroblasts, attenuating antitumor immunity, and facilitating tumor invasion.

CDH6 expression is elevated in RA FLS due to epigenetic and local conditions of synovitis promoting migration, survival and cell growth, which are characteristic features of aggressive RA FLS. The intracellular distribution suggests additional functions beyond adhesion and homotypic aggregation, such as signaling and gene regulation. These data suggest CDH6 contributes to RA pathogenesis by influencing pathologic FLS behavior and could be a therapeutic target.

Additionally, ADMET profiling confirmed favorable drug-like properties and acceptable pharmacokinetic characteristics of daidzin. Overall, this integrated analysis suggests that daidzin could serve as a promising natural agent for breast cancer chemoprevention by targeting and downregulating essential oncogenes and disrupting critical cancer-associated signaling pathways.

Additionally, elevated VCAN expression was correlated with poorer survival and a reduced response to anti-PD-1 immune checkpoint inhibitor treatment of GC. This study established a lncRNA-based risk model for predicting the prognosis of GC patients and identified a ceRNA mechanism involving AP000695.2-miR-144-3p-VCAN, presenting novel biomarkers and therapeutic targets for GC treatment.

Low SPIN1 expression group could benefit from Axitinib, Cytarabine, Pazopanib and Sunitinib. Finally, we screened the 10 genes with the strongest correlation with SPIN1, among which CDH11 and SLC8A1 were associated with the prognosis of GC. In conclusion, our study has provided valuable insights into the pivotal role of SPIN1 in GC development, elucidating its potential molecular mechanisms and establishing it as a promising therapeutic target.

CDH11 is a novel therapeutic target in ESCC, and its inhibition by celecoxib/DMC offers a promising strategy for ESCC treatment.

While somatic copy number alterations were universally more common to aggressive tumors, besides shared alterations impacting DDX3Y and USP9Y, African derived tumors were prone to somatic losses associated with KDM5D, PCDH11Y, and RBMY. This much-needed African inclusive study alludes to possible Y chromosome contribution, at least in part, to treatment resistance and worsened mortality rates in African men.

This study is the first to identify ALV-J resistance-associated genetic markers in Chengkou mountain chickens, revealing key genes related to immune regulation, membrane function, and tumor development. The findings provide a foundational molecular basis for disease-resistant breeding in poultry.

Celecoxib significantly inhibited clinical arthritis and bone progression in the joints of SKGc, but not etoricoxib (another COX-2i), nor naproxen (COX-2 nonselective). Of the NSAIDs, only celecoxib inhibited bone progression in SKGc and OB differentiation and bone mineralization in the BdCs of mice and AS patients via CDH11/WNT signaling, independent of the COX-2 inhibition. [BMB Reports 2025; 58(3): 140-145].