CD24 targets
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE46708 | GEO | 2014/05/05
SECONDARY ACCESSION(S): PRJNA202070
REPOSITORIES: GEO
Similar Datasets
Project description:Gene expression were identified with or without CD24 gene silencing in Du145 cells. RNA isolated from 5 independent cultures of Scramble control, 3 cultures of CD24-ShRNA1 and 2 cultures of CD24-ShRNA2 were tested using Affimatrx Human U133 Plus 2.0 microarrays.
2014-05-05 | E-GEOD-46708 | biostudies-arrayexpress
Project description:CD24 plays a crucial role in tumor growth and metastasis, including in prostate cancer. While CD24 stimulates prostate cancer cell growth by controlling the ARF-NPM interaction and p53 inactivation, the mechanism of CD24-mediated metastasis remains elusive. This study identifies a direct interaction between CD24 and RCC2 with roles in prostate cancer cell proliferation and migration. Immunohistochemical analysis of primary prostate cancer samples showed expression of CD24 in 49% of samples and RCC2 in 82%, with a positive correlation between their protein levels. Their co-expression, particularly the binding of CD24 to the C-terminal domain of RCC2, supports their direct interaction, which may regulate cell motility and adhesion. Functional assays revealed that knockout (KO) of RCC2 in DU145 and PC3 prostate cancer cells inhibited cell proliferation but unexpectedly enhanced cell migration and invasion, while CD24 KO reduced proliferation and migration. Notably, dual KOs of CD24 and RCC2 led to a significant decrease in cell proliferation but showed mixed effects on migration, indicating a complex interplay between these proteins. In vivo, RCC2 KO in prostate cancer cells promoted spontaneous lung metastasis without significantly altering primary tumor growth, contrasting with CD24 KO, which reduced tumor growth and metastasis. Mechanistically, RCC2 was shown to ubiquitinate and degrade Vimentin, influencing cytoskeletal dynamics and migratory behavior. Furthermore, CD24 was found to ubiquitinate and degrade RCC2, leading to modulation of the β-catenin signaling pathway. RCC2 KO increased β-catenin activation and decreased the expression of its inhibitors AXIN2 and APC, while CD24 KO led to β-catenin inactivation. This opposing regulation of β-catenin signaling by CD24 and RCC2 underscores their differential roles in prostate cancer cell migration. These findings provide new insights into the molecular mechanisms underlying prostate cancer growth and metastasis and identify the CD24-RCC2 axis as a potential therapeutic target for controlling tumor growth and metastasis in prostate cancer.
2025-07-21 | GSE277962 | GEO
Project description:Expression profiling of CD24+ and CD24- population cells from myeloma cell lines. Results provide insight into the role of CD24+ cells in myeloma development. Keywords: multiple myeloma, cancer stem cell, CD24
2020-10-31 | GSE109650 | GEO
Project description:CD24, or heat stable antigen, is a cell surface sialoglycoprotein expressed on immature cells that disappears after the cells have reached their final differentiation stage. CD24 may be important in human embryonic kidney epithelial cell differentiation. In mice, CD24 expression is up-regulated in the early metanephros and localized to developing epithelial structures but the role and expression of CD24 in the developing human kidney has not been well described. In normal human fetal kidneys from 8 to 38 weeks gestation, CD24 expression was up-regulated and restricted to the early epithelial aggregates of the metanephric blastema and to the committed proliferating tubular epithelia of the S-shape nephron; however individual CD24+ cells were identified in the interstitium of later gestation and postnatal kidneys. In freshly isolated cells, FACS analysis demonstrated distinct CD24+ and CD24+133+ cell populations, constituting up to 16% and 14% respectively of the total cells analyzed. Isolated and expanded CD24+ clones displayed features of an epithelial progenitor cell line. Early fetal urinary tract obstruction resulted in an upregulation of CD24 expression, both in developing epithelial structures of early gestation kidneys and in the cells of the injured tubular epithelium of the later gestation kidneys. These results highlight the cell specific expression of CD24 in the developing human kidney and dysregulation in fetal urinary tract obstruction. We used microarrays to define the differences in global gene expression between obstructed and normal human fetal kidneys.
2009-11-11 | GSE18969 | GEO
Project description:Type II germ cell tumors (GCTs) are with more than 90% the most common neoplasia in young men of age 14 - 45 years. It is generally accepted that GCTs arise from a common precursor lesion, called germ cell neoplasia in situ (GCNIS), eventually developing into seminomas or non-seminomas. The non-seminomatous stem-cell like embryonal carcinomas (EC) can further differentiate into teratomas (TE), yolk sac tumors (YST), or choriocarcinomas (CC). Orchiectomy followed by chemo- or radiotherapy is a widely used procedure in the treatment of type II GCTs, leading to high cure rates of up to 90%. Nevertheless, about 10 - 15% of patients with progressive disease relapse as a result of drug resistance and are condemned for a poor prognosis and a short survival of only a few months. Cluster of differentiation 24 (CD24) is a small, mucin-like glycosylphosphatidylinositol (GPI) anchored membrane molecule that functions both, in signal transduction and as an adhesion molecule. This glycoprotein is mainly expressed on the surface of hematopoietic, neural, muscular, and epithelial cells. Moreover, CD24 has been implicated in tumor metastasis, as fucosylated CD24 interacts with P- and E-selectin, allowing invasion of tumor cells to distal sites. High expression or amplifications of CD24 has been described in a variety of solid malignancies, such as non-small cell lung carcinoma, gliomas, breast cancer, retinoblastoma, hepatocellular carcinoma, renal cell carcinoma, cervical carcinoma, prostate cancer, urothelial carcinoma, pineal parenchymal tumors, and ovarian cancer. In this study, we investigated the putative function of CD24 and its interaction partners in (cisplatin-resistant) GCT cell lines by generating CD24-deficient EC cells by CRISPR/Cas9-mediated gene editing. Changes in the proteome between CD24-deficient cells and parental cells were measured by liquid-chromatography coupled with mass spectrometry (LS-MS).
2022-01-19 | PXD025110 | Pride
Project description:CD44+/CD24- subpopulation of normal and cancerous breast epithelial cells are suggested to have stem cell properties. The goal of this study was to identify gene expression differences between CD44+/CD24- and CD44-/CD24+ subpopulation of cells from a same cell lines. We selected MCF-10A cells, which are immortalized derived from a fibrocystic breast disease. These cells are immortalized but not transformed and express basal cell markers. Cells were from a single sort but plated into four 100 mm plates. RNA was prepared from each plate separately for the analysis. Comparison of gene expression between 2 groups ( CD44+/CD24- and CD44-/CD24+) 4 replicates each.
2010-03-07 | E-GEOD-15192 | biostudies-arrayexpress
Project description:CD44+/CD24- subpopulation of normal and cancerous breast epithelial cells are suggested to have stem cell properties. The goal of this study was to identify gene expression differences between CD44+/CD24- and CD44-/CD24+ subpopulation of cells from a same cell lines. We selected MCF-10A cells, which are immortalized derived from a fibrocystic breast disease. These cells are immortalized but not transformed and express basal cell markers. Cells were from a single sort but plated into four 100 mm plates. RNA was prepared from each plate separately for the analysis.
2010-03-01 | GSE15192 | GEO
Project description:Expression data from WT CD24+CD172a+ cDC2s, WT CD24–CD172+ cDC2s, and WT CD24+CD172a– cDC1s
| PRJNA548944 | ENA
Project description:We endeavored to identify factors and pathways regulated by CD24 and to obtain leads regarding the mechanism by which CD24 inhibited the invasiveness and metastasis of pancreatic cancer cells by performing cDNA microarray analysis on S2-013 CD24 RNAi clones and control clones. The group of genes showing increased expression was mainly comprised of genes for molecules with functions related to RNA metabolism, transcription factors, proteases, and molecules involved in embryonic development and cell growth. The set of genes downregulated by knockdown of CD24 included the target mRNAs of a phosphorylation-dependent endoribonuclease G3BP that interacted with CD24. The target mRNAs of G3BP were identified in GSE17056. These results suggested that CD24 inhibited the RNase activity of G3BP, and that a function of CD24 was to inhibit the degradation of specific mRNAs.
2009-07-23 | GSE17055 | GEO
Project description:We endeavored to identify factors and pathways regulated by CD24 and to obtain leads regarding the mechanism by which CD24 inhibited the invasiveness and metastasis of pancreatic cancer cells by performing cDNA microarray analysis on S2-013 CD24 RNAi clones and control clones. The group of genes showing increased expression was mainly comprised of genes for molecules with functions related to RNA metabolism, transcription factors, proteases, and molecules involved in embryonic development and cell growth. The set of genes downregulated by knockdown of CD24 included the target mRNAs of a phosphorylation-dependent endoribonuclease G3BP that interacted with CD24. The target mRNAs of G3BP were identified in GSE17056. These results suggested that CD24 inhibited the RNase activity of G3BP, and that a function of CD24 was to inhibit the degradation of specific mRNAs. Transcripts upregulated or downregulated by knockdown of CD24 were identified through expression profiling of a total of 12,135 genes in S2-013 CD24 RNAi clones compared to control clones. Before labeling with Cy5 or Cy3, total RNA from two S2-013 CD24 RNAi clones were mixed and total RNA from two control clones were mixed. The supplementary files 'GSE17055_higher_siCD24.txt' and 'GSE17055_higher_control.txt' list the differentially expressed genes.
2010-06-24 | E-GEOD-17055 | biostudies-arrayexpress