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Project description:BackgroundPluripotent stem cells (PSCs), including human embryonic stem cells (hESCs), hold great potential for regenerative medicine and cell therapy. One of the major hurdles hindering the clinical development of PSC-based therapy is the potential risk of tumorigenesis. CD133 (Prominin 1, PROM1) is a transmembrane protein whose mRNA and glycosylated forms are highly expressed in many human cancer cell types. CD133 also serves as a cancer stem cell (CSC) marker associated with cancer progression and patient outcome. Interestingly, CD133 is highly expressed in hESCs as well as in human preimplantation embryos, but its function in hESCs has remained largely unknown.MethodsCD133 knockout hESC WA26 cell line was generated with CRISPR/Cas9. CD133 knockout and wide type hESC lines were subjected to pluripotency, proliferation, telomere biology, and teratoma tests; the related global changes and underlying mechanisms were further systemically analyzed by RNA-seq.ResultsCD133 deficiency did not affect hESC pluripotency or in vivo differentiation into three germ layers but significantly decreased cell proliferation. RNA-seq revealed that CD133 deficiency dysregulated the p53, PI3K-Akt, AMPK, and Wnt signaling pathways. Alterations in these pathways have been implicated in tumor proliferation and apoptotic escape.ConclusionsOur data imply that CD133 could be an additional target and used as a selective marker to sort and eliminate undifferentiated cells in reducing potential teratoma formation risk of hESCs in regenerative medicine.
| S-EPMC7251672 | biostudies-literature
Project description:Role of CD133 in human embryonic stem cell proliferation and teratoma formation
| PRJNA589324 | ENA
Project description:Transcriptional profiling of CD133+/high vs CD133-/low cell populations of Caco2, HT-29 and HUH7 cell lines. Further in silico analysis of differentially expressed transcripts and proteins in CD133+/high vs CD133-/low cell populations revealed several potential key molecular regulators of CD133. In silico data was proved by CRISPR/CAS9 gene editing system.
2022-09-24 | E-MTAB-11779 | biostudies-arrayexpress
Project description:Renal repair after injury is dependent on clonal expansion of proliferation competent cells. In the human kidney, the expression of CD133+ characterizes a population of resident scattered cells with resistance to damage and ability to proliferate. However, the biological function of the CD133 molecule is unknown. We found by RNA sequencing that cells undergoing cisplatin damage lost the CD133 signature and acquired metanephric mesenchymal and regenerative genes such as SNAIL1, KLF4, SOX9 and WNT3. CD133 was reacquired in the recovery phase. Lack of CD133 was specifically correlated with deregulation of the Wnt signalling and E-cadherin pathway and, functionally, limited cell proliferation after injury. By immunoprecipitation, CD133 appeared to form a complex with E-cadherin and β-catenin. In parallel, CD133-Kd cells showed lower β-catenin levels in basal condition and after Wnt pathway activation and reduced TCF/LEF promoter activation in respect to CD133+ cells. Finally, the lack of CD133 impaired generation of nephrospheres while favored senescence. These data indicate that CD133 may act as a permissive factor for beta-catenin signalling, preventing its degradation in the cytoplasm. Therefore, CD133 itself appears to play a functional role in renal tubular repair trough maintenance of proliferative response and control of senescence.
2018-03-07 | GSE107273 | GEO
Project description:Several novel potential oncogenic and tumor suppressor miRNAs were identified by using the appropriate controls for stem cells. Expression profiles for human miRNAs in six samples were generated. The Agilent platform GPL7731 was used to analyze six RNA samples: CD133- human NPC, CD133+ human NPC, CD133- B4 glioma, CD133+ B4 Glioma, CD133+ NCH441 glioma, CD133+ NCH644 glioma
2013-08-02 | E-GEOD-49470 | biostudies-arrayexpress
Project description:6 benign TURP samples taken directly from patients were subjected to collagen digestion overnight. Epithelial cells isolated were adhered to collagen for 15 minutes. Adherent cells were passed through a magnetic bead column and cells positive for CD133 antibody were double selected. RNA was extracted from CD133+ and CD133- cells from each patient and amplified using the RiboAmp HS RNA amplification system. CD133+ (Cy5) and CD133- (Cy5) cDNA was hybridised to 30K cDNA array (CRUK facility) using the Invitrogen post labelling system. In each case that RNA was co-hybridised to a human pooled universal reference cDNA (Cy3). Keywords: repeat sample
2008-03-01 | GSE9935 | GEO
Project description:Epithelial cell cultures derived from benign and HRPC tissue biopsies were expanded in culture for 2-3 weeks. CD133+ and CD133- cells were isolated using the miltenyi magnetic bead system after adherence to collagen. CD133+ and CD133- RNA was isolated and amplified using the RiboAmp HS kit and expression profiling performed using the CRUK WGA gene set. Keywords: Tumour vs normal comparison
2008-03-01 | GSE9962 | GEO
Project description:We cultured tumor cells from 22 GBM under medium conditions favoring the growth of neural stem cells. 11 out of 15 primary GBM contained a significant CD133+ subpopulation that comprised cells showing all hallmarks of neural stem cells. Cell lines derived from these CD133+ GBM showed a neurosphere-like, non-adherent growth pattern. In contrast, 4 out of 15 cell lines derived from primary GBM grew adherent in vitro and were driven by CD133- tumor cells that fulfilled stem cell criteria. In vivo, these GBM were characterized by a significantly lower proliferation index but similar GFAP staining as compared to CD133+ GBM. Gene arrays from 2x3 representative cells lines are given. Keywords: Cancer stem cell, CD133, glioblastoma
2007-03-06 | GSE7181 | GEO
Project description:Gene expression profiling of CD44-CD133+ and CD44+CD133+ Caco2 population
2021-01-01 | GSE154750 | GEO
Project description:CD133 has been widely used for identification and isolation of cancer stem cells in tumors although its role as a marker for cancer stem cell is still controversial . We isolated the CD133+ and CD133- cells from SW620 human colon cancer cell line and compared their biological characteristics, such as tumorigenicity,drug sensitivity, etc. Our study revealed that CD133+ SW620 cells were more tumorigenic and resistant to anti-cancer drugs. Correspondingly, they displayed different gene expression profile. However, it was observed that CD133- cells and CD133+ cells could mutually convert, indicating that CD133 expression was under dynamic and reversible regulations which might impose significant infulence on cells behaviors. Thus, our data challenge the role of CD133 as a marker for cancer stem cell.
2010-07-29 | GSE23295 | GEO