CD24 expression

The OS average in the Grade I (P = 0.014) and Grade III (P = 0.004) groups was statistically lower than the OED group. Although more than half of the patients demonstrated high expression of both markers, there was no statistically significant difference between them and clinicopathological indices.

Moreover, in situ production of paramagnetic Mn2+ from the nanomedicine serves as an excellent contrast agent for magnetic resonance imaging (MRI) to monitor the therapeutic process. This study demonstrates that this multifunctional MRI-visible siCD24- and lenvatinib-loaded nanodrug holds great potential in enhancing therapeutic sensitivity for HCC lenvatinib therapy.

Moreover, ex vivo human tissue incubation with the probe supported the potential for intraprocedural lesion identification via topical probe application during colonoscopy. In conclusion, this study successfully demonstrates the potential of CD24-targeted NIR-II imaging for identifying colorectal neoplasia, highlighting its significance for early CRC detection in the gastrointestinal tract.

In addition, ACAT1 overexpression inhibited cell migration and invasion, improved the response to 5-Fluorouracil (5-FU) and etoposide. Correlation analysis indicated ACAT1 mRNA expression was correlated with immune infiltrates. Collectively, our data show that ACAT1 induces pronounced inhibitory effects on gastric cancer initiation and development, which may impact future strategies to treat this aggressive cancer.

Furthermore, using Akt inhibitor MK2206, we showed that Akt-signaling-driven SP1 drove the expression of the three LCSC markers Our findings suggest that Akt-signaling-driven SP1 promotes EPS8L3 expression, which is critical in maintaining the downstream expression of CD24, CD13 and EpCAM. The findings provide insight into potential LCSC-targeting therapeutic strategies.

Finally, IL21-AS1 increased CD24 expression in OC and facilitated OC progression. Our findings provide a molecular basis for the regulation of CD24, thus highlighting a potential strategy for targeted treatment of OC.

Anthropometric measures, such as birthweight, height, and childhood body fatness, may have long-term impacts on stem cell population in the breast.

Consequently, we show that bestatin, a clinically advanced aminopeptidase inhibitor, binds to GPAA1 and blocks GPI attachment, resulting in reduced CD24 cell surface expression, increased macrophage-mediated phagocytosis, and suppressed growth of ovarian tumors. Our study highlights the potential of targeting GPAA1 as an immunotherapeutic approach for CD24+ ovarian cancers.

While it caused a non-significant decrease in CD24 expression in cultured breast tumor tissue and a significant decrease in its expression in the corresponding normal ones. Anti-IL-8 monoclonal antibody exhibits promising immunotherapeutic properties through targeting both autophagy and CSCs maintenance within breast cancer TME.

(2) The expression of markers CD24, CD44, ALDH1, and ABCG2 was analyzed on the surface of CSCs in two cancer cell lines, MDA-MB-231 and HCT-116, after treatment with 5-fluorouracil (5-FU) using flow cytometry analysis...(4) Each individual GA prediction model achieved high accuracy in estimating the expression rate of CSC markers on cancer cells treated with 5-FU. Artificial intelligence can be used as a powerful tool for predicting drug resistance.

High TAM Siglec10 expression and tumor CD24 expression are correlated, and the high Siglec10+CD24 combination is a major risk factor for recurrence. CD68+Siglec10 TAMs are important prognostic factors. Siglec10 expression on TAMs is essential for tumor microenvironment immunoregulation and offers a promising new immunotherapeutic approach for lung adenocarcinoma.

In addition, we observed that VGLL1 represses AXL expression and suppresses claudin-low phenotype, and that is caused by the VGLL1 mediated nuclear expulsion of TAZ. Therefore, EGFR and AXL seem to represent two different breast tumor subtypes, and their differential expressions is controlled by VGLL1.

High expression of CD44 and CD24 will shorten the disease-free survival of patients with advanced ovarian cancer.

Our study demonstrates that the upregulation of CD133 is linked to cellular proliferation and protects PTC from apoptosis in DKD and high glucose induced PTC injury. We propose that heightened CD133 expression may facilitate cellular self-protective responses during the initial stages of high glucose exposure. However, its sustained increase is associated with the pathological progression of DKD. In conclusion, CD133 exhibits dual roles in the advancement of DKD, necessitating further investigation.

Further analysis using reverse-phase protein array and its validation using CD24-modulated TNBC cells and xenograft models nominated CD24-NF-κB-CPT1A signaling pathway as the central regulatory mechanism of CD24-mediated FAO activity. Overall, our study proposes a novel role of CD24 in metabolic reprogramming that can open new avenues for the treatment strategies for patients with metastatic TNBC.

Our results showed that CD24 expression may induce a cellular quiescence-like state and resistance to platinum-based chemotherapeutic agents in ovarian cancer via miR-130a and 301a upregulation. CD24-miR-130a/301a-CDK19 signaling axis could be a prognostic marker for or a potential therapeutic target against ovarian cancer recurrence.

Additionally, the high CD44v3 expression group, as determined by IHC, exhibited significantly decreased expression of U2 small nuclear RNA auxiliary factor 1 (U2AF1) at the mRNA level compared with that in the low CD44v3 expression group (P<0.001, Mann-Whitney U test), and U2AF1 and PD-L1 mRNA expression exhibited a significant negative correlation (τ=-0.3948, P<0.001, Kendall rank correlation coefficient). In conclusion, CSCs in OSCC may evade host immune mechanisms and maintain CSC stemness via PD-L1/PD-1 co-expression, resulting in unfavorable clinical outcomes.

Exploiting this viral sensitivity to CD24 offers the possibility of its use as a prognostic target for a broad population of expressing cancers, many of which have shown resistance to current clinical therapies. Sensitivity to the tumoricidal effect of ZIKV on high-risk neuroblastoma tumors is dependent on CD24 expression, offering a prognostic marker for this oncolytic therapy in an extensive array of CD24-expressing cancers.

Using a molecular docking approach, we demonstrated that sitagliptin targeted CD24/SOX4-centered signaling molecules with high affinity. In vitro experimental data showed that sitagliptin treatment suppressed CRC tumorigenic properties and worked in synergy with 5FU and this study thus provided preclinical evidence to support the alternative use of sitagliptin for treating CRC.

Our findings suggest inverse associations of CD44 in stroma and combined stromal + epithelial CD24 with BCa risk. Future studies are warranted to confirm our findings and to examine these associations by BBD subtype.

Together, our study provides a novel link between Hippo/YAP signaling and macrophage-mediated immune escape, which suggests that the Hippo-YAP-CD24 axis may act as a promising target to improve the prognosis of ESCC patients. A proposed model for the regulatory mechanism of Hippo-YAP-CD24-signaling axis in the tumor-associated macrophages mediated immune escape.

CD24 may attenuate the positive effects of high TIL levels on survival and may facilitate the immune escape of TNBC by regulating PD-L1 expression. Thus, it is a potential target for immunotherapy in TNBC.

CD24 is a possible uprising marker for tumor identification, overexpressed in PBLs and is intensely stained in tumor tissue and pre-malignant lesions. Tumor-PBLs should be further studied.

And, CD24 or MET knockdown or miR-181a overexpression inhibited the manifestation of CSC phenotypes, cellular quiescence-like state and chemoresistance, in OV90 and SK-OV-3 cells: increased colony formation, decreased G0/G1 phase cell population and increased sensitivity to Cisplatin and Carboplatin. Our findings suggest that CD24-miR-181a-MET may consist of a signalling route for ovarian CSCs, therefore being a combinatory set of markers and therapeutic targets for ovarian CSCs.

Cytoplasmic AR expression is associated with UCB invasiveness. Smoking history and CD24 expression were not associated with UCB invasion.

Furthermore, immunofluorescence and flow cytometry results indicated that both the single treatment group and combination treatment group enhanced the infiltration of immune cells. This study presents a novel approach to identifying combination therapy and targets for the clinical treatment of HCC with oxaliplatin.

Acknowledgments. GB was supported by Fundación Alfonso Martín Escudero.

Despite the advent of new agents such as ibrutinib and venetoclax that have dramatically changed the clinical fate of CLL, young patients still experience refractory and resistant disease, with few therapeutic options available over time...In this study, we explore the possibility of targeting CD24 in human primary samples of CLL (huCLL), redirecting the activity of NLCs against CLL cells using anti-CD24 mAb alone or in combination with other agents (anti-CD47, Rituximab)...Anti-CD24 mAb, in particular, showed the ability to redirect patient-derived NLCs' phagocytic activity to cognate huCLL cancer cells, resulting in higher clearance in cases of multiple combination. Boosting the autologous innate immune system might, therefore, provide further therapeutic options in the setting of CD24+ CLL, particularly for those patients who have failed several lines of treatment and have limited options available.

CD24 expression was high in granulocytes from MPN transformed into AML and in the JAK inhibitors ruxolitinib and fedratinib-resistant HEL cells (Nat Cancer 4:108). This treatment improved thrombocytosis, decreased platelet-neutrophil complexes, restored normal clearance of mutated senescent neutrophils and reduced emperipolesis levels which, in turn, decreased active TGF-β, ultimately improving myelofibrosis. This study reveals defective neutrophil clearance as a cause of pathogenic microenvironmental interactions that may increase thrombosis and myelofibrosis risk, and postulate CD24 as a candidate target for innate immune checkpoint in myeloid malignancies.

Similarly, unstimulated CLL patients-derived NLCs provided increased phagocytosis when DEMs blockade occurred. Since high levels of CD24 were associated with worse survival in both MCL and CLL, anti-CD24-induced phagocytosis could be considered for future clinical use, particularly in association with other agents such as Rituximab.

P1, N=48, Recruiting, ImmuneOnco Biopharmaceuticals (Shanghai) Inc. | Not yet recruiting --> Recruiting

Conclusions In preclinical studies, ATG-031 demonstrates potent antitumor activity, excellent safety and PK properties, which supports its further development in clinical trials. A phase I, multicentre, dose-escalating clinical trial is being developed to evaluate ATG-031 in patients with solid tumors and hematologic malignancies.

BVE‐Met cells developed resistance to BRAFV600E inhibitor PLX4720, but remained sensitive to β‐catenin/KDM4A inhibitor PKF118‐310. In summary, we have identified several targetable genes/pathways in thyroid cancer metastasis. Given the complexity of metastatic cells in evasion of host immune response, simultaneously targeting more than one of these pathways (PDL1, Mertk, IL6, COX‐1/Tbxas1‐TXA2) may be warranted to achieve better therapeutic effect.

CHOP and PERK overexpression promoted hypoxia-induced apoptosis of CD44CD24 cells (P<0.05), whereas mitochondrial membrane permeability inhibitors inhibited hypoxia-induced apoptosis of CD44CD24 cells overexpressed CHOP gene. CD44CD24 tumor stem cells in EC resist to hypoxia-induced apoptosis by the inhibition of ERS-mediated mitochondrial apoptosis pathway, which suggested that ERS pathway can serve as a potential target for reducing EC treatment resistance in clinical treatment.

Our findings have important implications in future practice, overexpression of CD24 in OSCC was associated with poor prognosis correlating to the clinical findings, large-scale comprehensive studies are needed further to confirm our findings. In addition to histological features, CD24 can be used as marker for OSCC.

CD44/CD24 profile may be used on small incisional biopsies to predict the outcome and treatment planning. This finding may help in developing new therapeutic targets to suppress cancer metastasis and provide a better long-term prognosis for patients diagnosed with OSCC.

Several of them seem to be interconnected as they initiate signalling down different pathways but converge at BCSC increase and tumor proliferation. This review highlights the common pathways between cachexia and BCSC signalling, to identify potential therapeutic targets that can aid both conditions.

Chemoresistant CD24/CD44GFP-ZEB1 cells depicted 1000-fold higher IC-50 values of doxorubicin and decreased activation of JNK-p38 stress kinase molecular signaling-dependent mammosphere forming efficiency to evade apoptosis. Thus, ZEB1 and its downstream effectors are plausible therapeutic targets for the mitigation of breast cancer chemoresistance in patients.

HER2/neu positive expression rate was 26.7% in the endometrial hyperplasia group and 57% in endometrial carcinoma group, with significant difference (p<0.05). In conclusion, aromatase P450 may be one factor associated with endometrial cancer cell proliferation, while CD24 and HER2/neu may be important factors associated with the invasion and metastasis of endometrial cancer.

P1, N=48, Not yet recruiting, ImmuneOnco Biopharmaceuticals (Shanghai) Inc.

Furthermore, we found that the CDKN2A gene may predict GBM sensitivity and resistance to drugs. Our findings suggest that CRGs play a crucial role in GBM outcomes and provide new insights into CRG-related target drugs/molecules for cancer prevention and treatment.

High CD44 and CD24 expression may be a predictor of poor response/nonresponse to neoadjuvant therapy in breast carcinomas. In recent years, stem cells have been defined as the main cell population responsible for resistance to anticancer therapies.