Ask about this productRelated genes to: CD133 antibody
- Gene:
- PROM1 NIH gene
- Name:
- prominin 1
- Previous symbol:
- PROML1, MCDR2, STGD4
- Synonyms:
- AC133, CD133, RP41, CORD12
- Chromosome:
- 4p15.32
- Locus Type:
- gene with protein product
- Date approved:
- 1999-04-15
- Date modifiied:
- 2016-10-05
Related products to: CD133 antibody
Related articles to: CD133 antibody
- Extracellular vesicles (EVs) are small nanometric particles surrounded by a lipid bilayer and actively secreted by different cell types. EVs play a key role in cell-to-cell communication, and the vast array of biomolecules that EVs transport reflects the molecular profile of the originating cells. In cancer, EVs are key components of the tumor microenvironment (TME); meanwhile once released into the peripheral circulation, EVs can travel systemically and transmit signals beyond the primary tumor site, making EVs ideal candidates for liquid biopsy. Notably, EVs can be isolated from a blood sample and analyzed to obtain real-time information on tumor biology, enabling early diagnosis, monitoring of treatment response, and evaluation of disease evolution, with high sensitivity and specificity. This review examines the biological significance and clinical utility of EVs expressing the stemness-associated glycoproteins CD44 and CD133 in gastrointestinal (GI) malignancies. Cancer stem cells (CSCs) expressing these surface markers are known to exhibit enhanced tumorigenic potential, metastatic capacity, and therapy resistance. In particular, we focus on the increasing evidence that EVs enriched in CD44+ and CD133+ populations play critical roles in key aspects of tumor progression in cholangiocarcinoma, pancreatic, colorectal, and gastric cancers. Following internalization by recipient cells, CD44+ and CD133+ EVs drive phenotypic reprogramming, foster more aggressive cellular states, and promote chemoresistance by delivering specific molecular cargo. Mechanistically, CD44 isoforms, particularly CD44v6 and CD44v9, activate key oncogenic signaling pathways, including Wnt/β-catenin and phosphoinositide 3-kinase (PI3K)/serine/threonine kinase AKT (AKT). In parallel, CD133-enriched EVs help maintain stemness and contribute to TME reorganization, thereby facilitating tumor progression. Despite ongoing challenges in EV isolation and standardization, EVs positive for stemness markers show great potential as liquid biopsy analytes for noninvasive disease monitoring, prognostic evaluation, and patient stratification. This review summarizes the expanding body of knowledge on cancer stem cell (CSC)-derived EVs in GI tumors, underscoring the potential of these particles for early diagnosis, prognosis, and the development of targeted therapies to overcome treatment resistance. - Source: PubMed
Pizzulli CristinaMenicacci BeatriceParrini MargheritaTonelli EdoardoBartolini CaterinaCurto ArmandoPetroni GiuliaPillozzi SerenaGalli Andrea - Head and neck mucosal melanoma (HNMM) arises in the nasal and oral cavities and has the propensity to metastasize to local and distant body sites. HNMM is also notable for its resistance to available therapeutics. The rarity of this disease makes it difficult to conduct large-scale clinical studies to develop standard treatment protocols. In contrast to cutaneous melanoma, c-Kit-dependent pathways are well studied in HNNMM and provide a potential therapeutic target. We identified and isolated genetically distinct subpopulations with stem cell characteristics in HNMM samples bearing Kit wild-type and mutations. Functional analysis of these subpopulations reveals that, in addition to expressing the stem cell marker proteins CD20, CD117, CD133, and CD166, these subpopulations are characterized by self-renewal potential, migratory capacity, and resistance to Kit inhibitors such as Imatinib. Immunofluorescence staining and inhibition experiments demonstrate that the maintenance and resistance of HHMM subpopulations to Kit inhibitors is mediated by the Kit signal to the PI3K signaling pathway. The KIT signal to the PI3K signaling pathway does not result exclusively from a KIT mutation localized to Exon 17, but can also be triggered by mutations localized to Exons 11 and 13. In the present study, we identify and characterize an HNMM subpopulation with stemness properties in patients with c-Kit wild-type and mutation, and demonstrate for the first time the mechanisms by which the CD117/CD133 HNMM subpopulations survive and confer resistance to the specific inhibitor of c-Kit mutation. - Source: PubMed
Publication date: 2026/04/19
Hassan Sofie-YasminSantourlidis SimeonFlanagan Thomas WHassan Sarah-LillyZhou HeSchmidt Morna FCacchi ClaudioLammert Matthias FerdinandMegahed MossadYazdi Amir SadeghJonigk Danny DavidAraúzo-Bravo Marcos JBrodell Robert TFacca SybilleHaikel YoussefHassan Mohamed - Breast cancer is the foremost cause of cancer-related death in women globally, and taxane-anthracycline (TA) combination regimens represent standard frontline chemotherapy. Although widely administered, the pathological complete response rate to TA therapy is less than 30%, and chemoresistance remains a major barrier to effective disease control, frequently leading to relapse and poor survival. Both metabolic reprogramming and tumor microenvironmental remodeling are closely associated with treatment failure, yet how they interact to drive TA resistance remains largely unclear. Here we show that phosphofructokinase platelet (PFKP), a key glycolytic enzyme, is highly expressed in breast cancer. PFKP drives glycolysis and promotes CD133 cancer stem-like cells (CSLCs) that are inherently TA-resistant. Moreover, PFKP-overexpressing cancer cells stimulate cancer-associated fibroblasts (CAFs), which in turn augment CD133 CSLC formation via the CXCL16/CXCR6 axis, establishing a feedforward loop that reinforces chemoresistance. These results reveal a previously unappreciated mechanism by which a glycolytic enzyme in cancer cells orchestrates stromal crosstalk to sustain a chemotherapy-refractory niche. By identifying PFKP as a key driver and the PFKP-CSLC-CAF axis as an actionable target, our work moves the field beyond the traditional view of metabolic reprogramming as a cell-autonomous event. Disrupting this axis-for instance, by PFKP inhibition or CXCL16/CXCR6 blockade-may restore TA sensitivity in aggressive basal-type breast cancer, offering a promising strategy to improve long-term outcomes for hard-to-treat patients. - Source: PubMed
Publication date: 2026/04/23
Fang KaiMa YueLi LihuaYue YanRuan HangXiong Sidong - Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that a section of the western blot image for β‑actin in Fig. 1B on p. 157 had also been used for the control β‑actin blots in Fig. 3C on p. 159, despite these data having come from different sources (Fig. 1: CD133 ovarian cancer cells compared with Fig. 3: CD133 ovarian cancer stem cells infected with recombinant adenovirus). In addition, upon performing an independent analysis of the data in this paper in the Editorial Office, it also came to light that, regarding the TUNEL assay experiments shown in Figs. 2 and 4, the data shown for panel '1' in Fig. 2D was strikingly similar to that shown for the 'Blank' panel in Fig. 4C, even though the experimental conditions in these figures were reported to be different. The authors have been contacted by the Editorial Office to offer an explanation for this apparent duplication of data within these figures, and we are waiting their response. Owing to the fact that the Editorial Office has been made aware of potential issues surrounding the scientific integrity of this paper, we are issuing an Expression of Concern to notify readers of these potential problems while the Editorial Office continues to investigate this matter further. [Oncology Reports 37: 155‑162, 2017; DOI: 10.3892/or.2016.5263]. - Source: PubMed
Publication date: 2026/04/17
Long QifangYang RuLu WeixianZhu WeipeiZhou JundongZheng CuiZhou DongmeiYu LingWu Jinchang - Mesenchymal stromal cells (MSCs) are widely used in human cell-based therapies and recent research is focused on the use of MSCs in equine regenerative medicine. Recently, MSCs have been isolated from equine follicular aspirates; however, a major concern during isolation is the potential contamination with fibroblasts, the predominant stromal cell type in many tissues. Furthermore, both cell types share the minimal criteria established by the International Society for Cellular Therapy (ISCT) for MSCs identification. Hence, our study aimed to compare the morphological characteristics, expansion behavior, immunophenotype, differentiation capacity and gene expression profiles of equine MSCs obtained from follicular aspirates and a commercial equine dermal fibroblast cell line. Under standard culture conditions, both cell lines exhibited a spindle-like morphology, expressed mesenchymal markers such as CD90 or CD29, and lacked the expression of CD45, CD19 and MHC-II, and manifested trilineage differentiation, however the chondrogenic differentiation was less evident in fibroblasts. Transcriptomic analysis using an RT² Profiler PCR Array revealed 35 differentially expressed genes between MSCs and fibroblasts. These results were further validated by quantitative PCR analysis: while fibroblasts showed higher expression of ANPEP, PROM1 and SOX2, genes like FGF2, LIF and KDR were downregulated in these cells. Moreover, GDF6, a key factor for MSCs differentiation, was markedly downregulated in fibroblasts. In conclusion, our results demonstrate that conventional criteria, including morphology, immunophenotyping, differentiation assays, and gene expression analysis, are insufficient to unequivocally identify MSCs. These findings underscore the need to implement additional experimental approaches to confidently discriminate between MSCs and fibroblasts. - Source: PubMed
Publication date: 2026/04/02
Del Prado Soriano-Campos MaríaMuñoz-García Carmen CristinaLuis-Calero MarcosGallardo-Soler AlejandroGonzález-Fernández LauroMacías-García Beatriz