CD24 (CD24 Molecule)

Further, we lyophilized and cryo-milled the decellularized tissue into a fine powder to fabricate a photo-cross-linked 3D hydrogel with tunable matrix crosslinking and rheology. Drug resistance was evaluated by culturing MDA-MB-231 cells encapsulated in 3D hydrogels with variable matrix crosslinking and rheology, and assessing the CD44+/CD24- cancer stem cell-associated phenotype linked to aggressiveness and therapy resistance.

Additionally, circRSU1 further enhances this process not only through increasing the hnRNPA1 protein level, but also through enhancing the interaction of hnRNPA1 with HIF1A IRES, consequently augmenting the CD24positive cell population and the associated malignancy/stemness features of HCC cells. Together, circRSU1 activates the hnRNPA1/HIF-1α/CD24 signaling axis, leading to the increased HCC malignancy and stemness features.

GNAL regulates the spatiotemporal immune remodeling of ER+ breast cancer via calcium signaling and stem-like cell differentiation. The multi-omics risk model offers clinical prognostic value and highlights GNAL as a potential target for precision immunotherapy.

Functional studies established that E2F2 directly regulates FZD10 expression, activating the Wnt/β-catenin pathway to sustain the stem-like state. Collectively, we unveil the E2F2/FZD10 axis as a previously unrecognized molecular conduit through which environmental arsenic reprograms mammary epithelial cells toward a BCSCs-like phenotype, providing mechanistic insight into arsenic-associated breast cancer risk and revealing a potential target for preventive intervention.

Activated CD24 promoted HCC formation through programmed death-ligand 1 signaling and could be a valuable biomarker for monitoring chronic liver disease malignancy.

Furthermore, CD24 knockdown reduced its expression level by promoting the ubiquitination modification of epidermal growth factor receptor (EGFR), and significantly inhibited its downstream AKT/mTOR signaling pathway. By interacting with EGFR and modulating the mTOR pathway, CD24 acted as a critical regulator of autophagic cell death, thereby enhancing the sensitivity of HER2+ BC cells and reversing Pyrotinib resistance.

Mechanistically, RD3 governs a self-reinforcing axis of cellular identity and immunoediting (by regulating T-cell cytokine release, activation, and cytotoxic function), positioning it as a critical checkpoint in NB evolution. These findings establish RD3 as a dual-function molecular switch and nominate RD3-targeted strategies to re-sensitize high-risk NB to immunotherapy.

We successfully tracked patient response to treatment by monitoring changes in glioma stem cell markers on circulating sEVs. We propose that these results provide a strong rationale for using GBM sEVs as a serial monitoring tool in the future clinical management of patients with GBM.

After isolation of stem cells from these cells by incubation with 5-fluorouracil (5-FU) and cisplatin (Cis), CSCs were identified by flow cytometry using CD24/CD44/CD133/EPCAM by assessing the rhodamine 123 (Rho 123). In conclusion, studying surface receptors and rhodamine uptake for the identification of CSCs is a powerful and valuable method for evaluating the efficacy of chemotherapy. The discovery of CSC markers that indicate therapeutic strategies could lead to clinical trials of medicines with potentially better therapeutic outcomes, particularly for recurring malignancies.

Finally, we identify the sulfotransferase enzyme GAL3ST4 as a potential driver of immune evasion in glioma cells. Our study provides a unique genomic atlas of cancer-associated glycosylation and identifies immediately actionable targets for cancer immunotherapy.

CD24 and CD133 exhibit high positive detection rates in GC tissues, and their co-positivity is closely associated with tumor stage progression and significantly indicates unfavorable survival outcomes. The co-expression of CD24/CD133 may reflect higher aggressiveness and metastatic potential of GC, serving as a potential prognostic marker and a direction for targeted therapeutic strategies. However, as this is a single-center retrospective study with limitations such as patient loss to follow-up and sample size, further prospective, multicenter, and mechanistic studies are required to validate its clinical applicability and biological role.

Hypoxia-induced oxidized ATM maintains TNBC-CSC stemness by promoting c-Myc-dependent upregulation of MTHFD2 and SHMT2, linking hypoxia, redox signaling, and one-carbon metabolism. These findings suggest a potential therapeutic axis that could be exploited for TNBC treatment.