CD44 (CD44 Molecule)

In vivo, GPX2 overexpression accelerates tumorigenesis, whereas targeting CCR3 with ALK4290 sensitizes tumors to anti-PD-1 checkpoint blockade. These findings delineate a dual mechanism whereby GPX2 couples oxidative stress regulation to immune modulation, positioning the GPX2-B cell axis as a promising therapeutic target for HBV-driven liver cancer.

Additionally, we found that differences in pre-treatment gene expression states can lead cells within the same treatment condition to follow divergent paths toward their ultimate resistance fate. This work provides a framework for extracting targetable gene expression states from complex resistance dynamics to eliminate multi-treatment resistance.

In translational models, HA/ZGA achieves potent tumor regression, suppresses metastasis, and establishes immunological memory against rechallenge. Our work redefines ZIF-8 as a therapeutic chameleon that dismantles mitochondrial energetics, ablates stemness, and reignites antitumor immunity, exemplifying nanomaterial repurposing to bridge metabolic intervention with immune potentiation.

In-vivo studies conducted on Balb/c mice showed reduced Psoriasis Area Severity Index, Spleen weight as well as reduced keratinocyte proliferation in histopathological studies. In conclusion, developed novel formulation of Albendazole reduced keratinocyte proliferation making it a possible effective strategy in the management of psoriasis.

High-throughput drug screening indicates broad therapeutic resistance within the CSC compartment. Through the comprehensive characterization of BCBM-derived CSCs, this study establishes a clinically relevant model that identifies CSCs and the MIC subpopulation as key drivers of brain metastatic progression and as promising targets for the development of effective therapeutic strategies.

In conclusion, PrP knockdown may sensitize resistant SCLC cells to doxorubicin and promote autophagy. These findings support PrP silencing as a promising strategy to reverse chemoresistance in SCLC.

Blue light irradiation reduced viability and migration in both OSCC cell lines and induced apoptosis only in non-metastatic SCC9 cells. Blue light exerted anti-tumor effects without promoting cancer stem cells properties, while decreasing their ability to self-renew.

HA-decoration was found to cause a formation of thicker corona and enrichment of plasma-derived protein corona components. These findings highlight the role of HA in enhancing CD44-mediated EV targeting and modulating the composition of protein corona.

Collectively, p40 is an initial signal for squamous metaplasia development from morular and Sur Ca cells, by modulating CSC properties. This leads to terminal squamous differentiation through the MYH9 monomer-polymer equilibrium, regulated by EBP50 and S100A4 under hypoxic conditions.

OCT4 expression is a specific biomarker for PDAC. Its increased expression signified PDAC progression and CD24 activation in a subset of PDAC. KRAS mutants have lower OCT4 expression, suggesting an alternative mechanism for cancer progression than that in OCT4 positive PDAC.

The system consisted of hollow copper sulfide nanoparticles loaded with 4-methylumbelliferone, modified with polymetformin, and surface-coated with hyaluronic acid to ensure targeted delivery via CD44 receptors...Furthermore, immunostaining confirmed that apoptosis, macrophage repolarization, and immune activation were increased. This research presents a synergistic nanoplatform that integrates matrix remodeling, photothermal therapy (PTT), and immune reprogramming, offering a promising strategy for treating metastatic and immune-evasive breast tumors.

When this interaction was blocked by LF3, AGEs-induced CD44 upregulation was reduced, and pathological angiogenesis and BM abnormalities were partially restored. These findings suggest that AGEs upregulate endothelial CD44 expression via β-catenin/TCF4 signalling pathway, which in turn promotes MMP9-mediated excessive degradation of BM components, leading to structural disorganisation and impaired vascular maturation in pathological angiogenesis.