LGALS3 (Galectin 3)

Furthermore, overexpression of Gal-3 and GPC-6 reverses the pro-apoptotic effect of ESPPW, as indicated by restored cycle regulatory proteins (CDK2) expression. In conclusion, these data demonstrate that ESPPW suppresses PDAC cell growth by promoting apoptosis and disrupting the functional activity of Gal-3 and GPC-6.

RGDfV or eptifibatide inhibited Gal3 binding to αvβ3 and αIIbβ3, respectively, but lactose, pan-galectin inhibitor, did not inhibit Gal3 binding to integrins...Known anti-inflammatory agents, Ivermectin, NRG1, and FGF1 inhibited integrin activation induced by Gal3 in αvβ3 and αIIbβ3. These findings suggest that Gal3 binding to site 2 may be a potential mechanism of pro-inflammatory and pro-thrombotic action of Gal3.

The higher Gal-3 expression and nuclear staining in OSCC may explain its aggressive nature. Gal-3 could be a diagnostic and prognostic biomarker due to its increased expression in cancerous tissues compared to normal samples.

Protein EpiScores are significantly associated with CRC survival. These findings highlight biological pathways underlying CRC prognosis and support the utility of Protein EpiScores for modeling survivorship.

Lysosome inhibitor chloroquine was employed to elucidate the underlying mechanism in vitro...Importantly, PPS-ELNs displayed an excellent safety profile in vivo. PPS-ELNs inhibit CRC progression through the lysosome-mediated mitophagy pathway.

In conclusion, our findings establish GAL3 and PDEδ, two KRAS-associated proteins, as promising combinatorial drug targets. Targeting these modulators provides an effective alternative strategy to overcome resistance mechanisms and enhance the clinical utility of existing KRAS inhibitors.

Although preclinical evidence shows that elevated intracellular Gal-3 protein levels promote drug resistance in CML, these findings have not yet been confirmed at the clinical level. This review underscores that both galectins are critical regulators of CML pathophysiology and highlight their potential as therapeutic targets to overcome TKI resistance.

Auranofin, an FDA-approved antirheumatic agent, reduces HBsAg secretion via lysosomal damage.

Psychosocial stress significantly worsens DOX-induced cardiotoxicity by promoting cardiac dysfunction, fibrosis, and maladaptive gene expression. This study highlights psychosocial stress as a critical risk factor for adverse cardiovascular outcomes in cancer patients receiving potentially cardiotoxic chemotherapy.

The patent landscape is dominated by β-D-galactopyranose and thiodigalactoside scaffolds, with limited innovation and unresolved issues in selectivity, drug-likeness, and efficacy, highlighted by GB0139's Phase II failure...Yet, robust biochemical data and structural proof of binding remain scarce. To move the field forward, future patents must diversify chemotypes, substantiate binding modes with crystallography or NMR, and demonstrate translation in relevant disease models.

We also show that transcriptional and immunological signatures suggest that galectins may regulate glioblastoma immunosuppression, extracellular matrix remodelling, and protein homeostasis. Our findings provide novel insights into the oncogenic and immunoregulatory roles of galectins in glioblastoma, establishing their potential as prognostic biomarkers and therapeutic targets.