CD24 overexpression

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.

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.

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.

Acknowledgments. GB was supported by Fundación Alfonso Martín Escudero.

CD24 and CD200 are overexpressed across diverse cancer types and serve as signaling checkpoints by engaging their respective receptors, Siglec-10 and CD200 receptor, which are expressed on tumor-associated myeloid cells. In this review, we summarized and discussed the latest advancements and insights into CD24 and CD200 as emergent immune checkpoint moieties, further delving into their therapeutic potentials for cancer treatment.

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.

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.

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.

Upon triggering immunogenicity with X-ray radiation, our hydrogel encapsulating efferocytosis inhibitor MRX-2843 enabled a cascade regulation to orchestrate polarization, efferocytosis, and phagocytosis of peritoneal macrophages for realizing robust phagocytosis of tumor cells and powerful antigen presentation, offering a potent approach for ovarian cancer therapy via bridging the innate effector function of macrophages with their adaptive immune response. Moreover, our hydrogel is also applicable for potent treatment of inherent CD24-overexpressed triple-negative breast cancer, providing an emerging therapeutic regimen for the most lethal malignancies in women.

Compared with low expression of CD24 gene, high expression of CD24 gene was an independent risk factor for the prognosis of MPM patients (HR=2.412, 95%CI: 1.291-4.492, P=0.006) . CD24 gene and protein are highly expressed in MPM tissues, and the high expression of CD24 gene suggests poor prognosis in MPM patients.

Our data has also confirmed that IMM47 specifically binds to and induces ADCC (antibody-dependent cellular cytotoxicity) ,ADCP (antibody-dependent cellular phagocytosis), and CDC (complement-dependent cytotoxicity) against a variety of cancer cells. Taken together, our data show that targeting CD24 on tumor cells using our IMM47 antibody may serve as potent immunotherapy for multiple cancer indications.

ATG-031, a first-in-class anti-CD24 antibody, demonstrated potent anti-tumor activity in vivo, re-polarizing M2-like TAM to anti-tumor M1 subtype in the TME and induced systemic anti-tumor immunity. A clinical study to investigate the safety and efficacy of ATG-031 in cancer patients is being developed.

These results highlight the low or absence of mRNA levels of the canonic targetable ICs in medulloblastomas. Importantly, the analysis revealed overexpression of CD24 and CD276, which can constitute prognostic biomarkers and attractive immunotherapy targets for medulloblastomas.

In summary, CD248 de-represses Wnt signaling and upregulates OPN and SERPINE1 in pericytes, resulting in enhanced angiogenesis and lung cancer growth. This novel axis of CD248-Wnt signaling-angiogenic factors in pericytes provides a potential target for lung cancer therapy.

In vivo studies to further understand the translational significance of this metabolic axis is underway. Taken together, our study demonstrates, for the first time, that CD24 presents a novel metabolic vulnerability that can target BCSCs to gain a therapeutic advantage in the treatment of drug-resistant TNBC patients.

It demonstrates potent in vivo anti-tumor tumor efficacy, suggesting promising therapeutic strategies against a broad range of solid tumor or hematological malignancies, which warrants further clinical investigation. A clinical study to investigate the safety and efficacy of ATG-031 in cancer patients is being developed.

By activating the hsa04650 and hsa04660 pathways, the expression of interferon gamma, interleukin (IL)-2, and IL-10 is promoted, which in turn improves the tumor immune monitoring ability of the body, induces tumor cell apoptosis, and inhibits tumor cell growth. CD247 is a potential target for improving the clinical treatment effect of HNSC and the prognosis of patients.

Targeting CD24 could enhance anti-tumor immune response by inhibiting TAMs.

In this research, CD24 cells accounted for the vast majority of TNBC cells, and they were insensitive to Taxol but sensitive to ferroptosis agonists and effectively escaped phagocytosis by tumor-associated macrophages...This system achieved dual antitumor effects, ultimately promoting cell death and thus inhibiting TNBC tumor growth, with some tumors even disappearing. The composite nanoprecision treatment system reported in this paper is a potential strategic tool for future use in the treatment of TNBC.

Five bioactive compounds (prostaglandin J2, tanespimycin, semustine, 5182598, and flunarizine) were identified using Connectivity Map. Thus, the results of this study indicate potential biomarkers that could have applications in the development of immune therapy for breast cancer. However, more in vivo, and in vitro studies are required to further verify these results.

CAR-T cells were detected by flow cytometry using the RQR8-specific CD34 antibody. The BCMA-CD24 CAR was found to be expressed on roughly 13% of T-cells. To determine the selective lysis by the CAR-T cells, we performed co-culture killing assays in which MM cell lines over-expressing CD24 (ARP-1 CD24OE or OCI CD24OE cells) were incubated with CAR-T cells.

Hsp70 may regulate CD24 expression. Co-expression of CD24 and Hsp70 may be a prognostic biomarker for lung cancer.

In a CRISPR/Cas9-deficiency model, we demonstrate that CD24 fulfils a bivalent role in differentiation via regulation of homeobox, phospho- and glycoproteins, i.e. it is involved in suppressing the germ cell/spermatogenesis program and mesodermal/endodermal differentiation, while poising the cells for ectodermal differentiation. Finally, blocking CD24 by a monoclonal antibody enhanced sensitivity towards cisplatin in EC cells, including cisplatin-resistant subclones, highlighting CD24 as a putative target in combination with cisplatin.

Moreover, overexpression of ELF5 in MCF-7 cells significantly increased both the mRNA and protein levels of CD24, while knockdown of CD24 expression restored cell proliferation, migration and invasion through adaptive ELF5 expression in MCF-7 cells. Therefore, these data suggest that ELF5 inhibits migration and invasion of breast cancer cells by regulating CD24 expression, which make provides a molecular mechanism for ELF5 to inhibit breast cancer from a new perspective and provides further theoretical support for the treatment and prevention of breast cancer.

CD24 was correlated with better R-CHOP treatment response and tumor immunosuppression in ABC-DLBCL. CD24 may be a promising signal in treatment and prognosis evaluation in ABC-DLBCL patients.

NPM/B23 silencing enhanced phagocytosis by macrophages through decrease of CD24 on cancer cells. Restoration of CD24 expression in NPM/B23-silenced cancer cells inhibited macrophage-mediated phagocytosis.

The Kaplan-Meier estimates of OS were significantly different in patients positive for CK-19 (p = 0.028), CD44/CD24 (p = 0.002), ALDH1/CD24 (p = 0.007) and HER2-positive (p = 0.022). Our results indicate that combined gene expression analysis in EpCAM CTCs provides prognostic information in MBC.

Overall, our results demonstrated a significant CD24 overexpression in human and canine prostate cancer, although its prognostic value may be questionable. However, tumors overexpressing CD24 may be a reliable model for new target therapies and dogs could be used of a unique preclinical model for these studies.

Luciferase promoter assays using the wildtype and mutated ERG binding site within the CD24 promoter showed ERG-dependent activation. Collectively, our results suggest that promoter DNA methylation of the CD24 gene and T2E fusion status are factors involved in the upregulation of CD24 in patients with PCa.

CD24 genetic variant might be of clinical value for risk assessment as part of cancer prevention programs. Further study on larger populations is needed to validate the importance of this dinucleotide deletion in CRC development. Overexpression of CD24 protein occurs early along the multistep process of CRC carcinogenesis, and a simple blood sample based on CD24 expression on peripheral blood leukocytes can contribute to early diagnosis.