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Prospects of antibodies targeting CD47 or CD24 in the treatment of glioblastoma.

ABSTRACT: Glioma is a malignant tumor with the highest incidence among all brain tumors (about 46% of intracranial tumors) and is the most common primary intracranial tumor. Among them, glioblastoma (GBM) is highly malignant and is one of the three refractory tumors with the highest mortality rate in the world. The survival time from glioblastoma diagnosis to death is only 14-16 months for patients with standard treatment such as surgery plus radiotherapy and chemotherapy. Due to its high malignancy and poor prognosis, in-depth studies have been conducted to explore effective therapeutic strategies for glioblastoma. In addition to the conventional surgery, radiotherapy, and chemotherapy, the glioblastoma treatments also include targeted therapy, immunotherapy, and electric field treatment. However, current treatment methods provide limited benefits because of the heterogeneity of glioblastoma and the complexity of the immune microenvironment within a tumor. Therefore, seeking an effective treatment plan is imperative. In particular, developing an active immunotherapy for glioblastoma has become an essential objective in the field. This article reviews the feasibility of CD47/CD24 antibody treatment, either individually or in combination, to target the tumor stem cells and the antitumor immunity in glioblastoma. The potential mechanisms underlying the antitumor effects of CD47/CD24 antibodies are also discussed.

SUBMITTER: Wu H

PROVIDER: S-EPMC8446212 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:CD24 is a potential oncogene reported to be overexpressed in a large variety of human malignancies. We have shown that CD24 is overexpressed in 90% of colorectal tumors at a fairly early stage in the multistep process of carcinogenesis. Anti-CD24 monoclonal antibodies (mAb) induce a significant growth inhibition in colorectal and pancreatic cancer cell lines that express the protein. This study is designed to investigate further the effects of CD24 down-regulation using mAb or small interfering RNA in vitro and in vivo. Western blot analysis showed that anti-CD24 mAb induced CD24 protein down-regulation through lysosomal degradation. mAb augmented growth inhibition in combination with five classic chemotherapies. Xenograft models in vivo showed that tumor growth was significantly reduced in mAb-treated mice. Similarly, stable growth inhibition of cancer cell lines was achieved by down-regulation of CD24 expression using short hairpin RNA (shRNA). The produced clones proliferated more slowly, reached lower saturation densities, and showed impaired motility. Most importantly, down-regulation of CD24 retarded tumorigenicity of human cancer cell lines in nude mice. Microarray analysis revealed a similar pattern of gene expression alterations when cells were subjected to anti-CD24 mAb or shRNA. Genes in the Ras pathway, mitogenactivated protein kinase, or BCL-2 family and others of oncogenic association were frequently down-regulated. As a putative new oncogene that is overexpressed in gastrointestinal malignancies early in the carcinogenesis process, CD24 is a potential target for early intervention in the prevention and treatment of cancer. The study compared gene expression profiles between human CRC cells HT29 before and after expression of 1 and 2 shRNA vectors directed at the human CD24 gene, GFP control gene, HT29 cells and Colo357, human pancreatic cancer cells, before and after the inhibition of the CD24 molecule using 72h treatment with anti-CD24 monoclonal antibodies.

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Prospects of antibodies targeting CD47 or CD24 in the treatment of glioblastoma.

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