DSG2 (Desmoglein 2)

Functional co-culture assays showed that myCAFs enhanced CSC-associated phenotypes in DSG2^high tumor cells in an MMP-dependent manner. Collectively, these findings delineate a spatially organized DSG2+CSC-myCAF niche that contributes to therapeutic resistance in NSCLC.

Pyrintegrin reversed the inhibitory effects of DSG2 knockdown on lung adenocarcinoma cells. DSG2 inhibits anoikis in lung adenocarcinoma cells by activating the integrin β1/FAK signaling pathway, thereby promoting cell proliferation and invasion.

In an external validation cohort, an area under the curve (AUC) of 0.922 for low-grade ccRCC detection and 0.874 for high-grade ccRCC detection was achieved, respectively, using urinary EVs. Furthermore, integrating single-cell sequencing data revealed that SERPINA1 and VEGFA in low-grade ccRCC, and APOC1 and TGFBI in high-grade ccRCC, were derived from tumour-associated macrophages, whereas NDUFA4L2 originated from cancer cells in both low- and high-grade ccRCC.

Our findings reveal the molecular mechanism by which TROP2 promotes migration, highlighting the critical role of intercellular junction integrity in cancer progression. These insights provide a foundation for developing targeted therapies against TROP2 and its associated signaling mechanisms in epithelial malignancies.

Formulations are well-tolerated at a 20 mg/kg dose. As another approach for refinement of the formulation for siRNA delivery, the lipid-coated pSiNPs are functionalized using an anti-human desmoglein-2 monoclonal antibody (aDSG2) to achieve better transfection efficacy.

Hirudin inhibits hematogenous metastasis of breast cancer through suppression of HIF-1α-controlled DSG2-mediated desmosome junctions, ultimately leading to the disintegration of CTC clusters. Our findings highlight the therapeutic potential of targeting HIF-1α-controlled DSG2-mediated desmosome junction conversion and position hirudin as a promising CTC clusters dissociator optimized for the clinical prevention of breast cancer metastasis.

This study highlights key cellular and molecular mechanisms underlying bladder cancer progression Post-BCG treatment. Through single-nucleus RNA sequencing, we identified critical TME subtypes, TGF-β signaling involvement, and crucial ligand-receptor interactions such as DSC2-DSG2 and ENG-BMPR2, which may serve as preliminary biomarkers requiring confirmation in larger independent cohorts. These findings offer valuable insights into enhancement of treatment strategies and patient outcomes.

While the presence of this gene cannot be directly linked to the presence of a myxoma, the possibility of a genetic association is relevant. Further research and broader genetic screening in such cases can possibly uncover a potential link and aid in the further understanding of atypical cardiac tumour biology.

Diminished DSG2 expression is correlated with reduced survival rates in CC patients, suggesting that DSG2 could serve as a potential prognostic biomarker for CC.

We demonstrate that P-cadherin and Desmoglien-2 interact robustly by swapping flexible portions of their protein backbone and that this molecular complex nucleates desmosome formation. Our results resolve the biophysical basis by which different adhesive proteins interact and mediate stable desmosome assembly.

Furthermore, we found that the IL-8/CXCR2 axis interacts with DSG2 to promote PCSC stemness and gemcitabine resistance by activating the Wnt/β-catenin pathway. These findings highlight the novel regulatory mechanism of DSG2 in PC, providing new targets for the development of therapeutics targeting PCSC niches.