CD9 (CD9 Molecule)

Drug likeness analysis results revealed that chalcone derivatives CD5, CD8, and CD9 and reference standard drugs lorlatinib and topotecan showed no violations against all five drug likeness rules. Current study overcomes these challenges by employing green nanocatalysts (Al(OH)₃ and Ti/Fe@Al(OH)₃) for eco-friendly, high-yield synthesis and computational screening to design potent, multi-target lung cancer therapeutic chalcone compounds. The online version contains supplementary material available at 10.1007/s40203-026-00599-3.

In vivo in orthotopic tumors formed by FC1199 cells GAL decreased CD9+-NK frequency, promoted M1-macrophage polarization, and activated NK and CD8+T-cells, together with a significant reduction of tumor weight, fibrosis and inhibition of angiogenesis. Our study identifies CD9+NKs as a novel cell subset expanded in PDAC and underscores the role of TGF-β1/TGF-βR1 signalling in promoting a pro-tumoral NKs GAL-treatment emerges as immunomodulator able in re-educating pro-tumor NKs cells in PDAC.

These findings indicate that urinary EVs provide highly pure vesicles with superior DNA quality, making them a robust and completely non-invasive source for molecular profiling. Urinary EV-DNA-based MRD assessment shows significant prognostic value and may serve as a practical tool for postoperative monitoring and risk stratification in colorectal cancer.

Integrated EV and serological profiling may enable minimally invasive differentiation between HCC and iCCA within LR-M lesions. By transforming ML-guided model discovery into a clinically interpretable paper-and-pencil additive score, we illustrate a translational pathway from computational discovery to practical application.

The BiacoreTM biosensor is able to directly detect and molecularly profile EVs in buffer and spiked in cell culture supernatant supplemented with 10% EV-depleted serum. Altogether, our findings illuminate the potential of SPR BiacoreTM technology in EV-related research as well as reveal the diagnostic potential of EV-associated CXCR4, offering valuable insights and paving the way for medical applications in diseases associated with aberrant CXCR4 expression.

Mrep exerted pathological effects by secreting activin A in a model of genetically induced heterotopic ossification (HO), which was suppressed by TLR4 inhibition. Thus, this study elucidates the context-dependent functions of macrophages and the link between injury and HO, suggesting that Mrep is a potential therapeutic target for regenerating muscles and suppressing HO.

Proof-of-concept was gained for the detection of PSMA-positive EVs in urine from prostate cancer patients and discrimination of breast cancer patients from healthy donors by quantifying EpCAM- or HER2-positive EVs in blood plasma. In conclusion, using low-volume biofluids, the one-step AF4-MALS-FLD workflow holds potential for fast and robust EV biomarker detection.

Hypoxia induces distinct exosomal miRNA signatures in skeletal muscle, regulating genes involved in differentiation, migration, and stress response. These findings suggest that exosome-mediated miRNA signaling contributes to hypoxia-driven muscle adaptation and intercellular communication.

This study presents a proof-of-concept for fully synthetic, protein-functionalized FSEMs as dual carriers for both chemical and gene-based agents, offering a safer and potentially more effective alternative to traditional cationic liposomes. These results lay the groundwork for future in vivo validation and translational cancer research.

Also, to successfully detect markers, e.g. Hsp70 or CD44, in serum EVs we demonstrated to require more intense sample preparation in specific assays. While more patient studies are needed in the future, this pilot study paves the way for understanding the molecular differences in the DLBCL subtypes and for detecting them in the lymphoma EVs.

These effects required both Na+/K+-ATPase-dependent endocytosis and autophagy, as rapamycin-induced autophagy alone did not remove surface CD63. Our findings reveal a previously unrecognized mechanism in which cardiac glycoside regulates EV cargo composition by coupling Na+/K+-ATPase-mediated endocytosis with autophagy. Given that endogenous and therapeutic cardiac glycosides are implicated in cardiovascular and cancer biology, this mechanism may broadly influence EV-mediated intercellular communication and represent a potential target for modulating EV functions.

Elevated PDGF-B reversely stimulates TGFBI production in macrophages, which creates a positive feedback loop. This TGFBI-mediated interaction between HSCs and macrophages remodels the profibrotic microenvironment to promote liver fibrosis, identifying a potential therapeutic target.