The clinicopathological significance of CD133 and Sox2 in astrocytic glioma

Abdelrahman, Aziza E; Ibrahim, Hanaa; Elsebai, Eman; Ismail, Eman I.; Elmesallamy, Wael Abd Elrahman Ali

doi:10.3233/cbm-181460

Cited by 9 publications

(19 citation statements)

References 52 publications

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“…In addition, the negative impact of Nestin on survival has also been observed in lung cancer, esophageal squamous cancer, bladder cancer, etc . Whereas in astrocytic tumor, the tumor of the central nervous system, the effects of CD133 and Nestin on prognosis are only discovered in a small volume of literatures . Therefore, this present study recruited relatively more patients with astrocytic tumor compared with the previous literatures and aimed to further validate the clinical relevance of CD133 and Nestin in astrocytic tumor regarding their impact on survival.…”

Section: Discussionmentioning

confidence: 85%

“…In brain tumors, CD133 is first used to identify cancer stem cells in pediatric samples of glioma and medulloblastoma, and CD133 positive tumor cells are more aggressive and with higher capacity to self‐renew . And in astrocytic tumor, CD133 expression is correlated with higher histological grade and larger tumor size . In addition, Nestin is one of the type VI intermediate filament proteins.…”

Section: Discussionmentioning

confidence: 99%

“…9,17 And in astrocytic tumor, CD133 expression is correlated with higher histological grade and larger tumor size. 18 In addition, Nestin is one of the type VI intermediate filament proteins. It regulates the stemness of different cancer cells and promotes tumor invasion and metastasis.…”

Section: Discussionmentioning

confidence: 99%

“…[24][25][26] Whereas in astrocytic tumor, the tumor of the central nervous system, the effects of CD133 and Nestin on prognosis are only discovered in a small volume of literatures. 18,19 Therefore, this present study recruited relatively more patients with astrocytic tumor compared with the previous literatures and aimed to further validate the clinical relevance of CD133 and Nestin in astrocytic tumor regarding their impact on survival. We disclosed that CD133 and Nestin both predicted poor OS in patients with astrocytic tumor.…”

Section: Discussionmentioning

confidence: 99%

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Clinical significance of CD133 and Nestin in astrocytic tumor: The correlation with pathological grade and survival

Zhang

Chen

et al. 2019

Clinical Laboratory Analysis

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Background We aimed to investigate the interaction between CD133 and Nestin and further assessed the correlation of CD133 and Nestin with clinicopathological characteristics and survival in patients with astrocytic tumor. Methods Totally 127 patients with astrocytic tumor underwent surgical resection were enrolled. Patients’ age, gender, and World Health Organization (WHO) grade were recorded, and the survival data were extracted from the follow‐up records. The expressions of CD133 and Nestin in astrocytic tumor tissues were analyzed by immunohistochemistry assay. The WHO grade I and II astrocytic tumors were defined as low‐grade astrocytic tumors (LGA), the WHO grade III and IV astrocytic tumors were defined as high‐grade astrocytic tumors (HGA). Results There were 79 (62.2%), 34 (26.8%), 14 (11.0%), and 0 (0.0%) patients with CD133 negative, low, moderate, and high expression, respectively; 7 (5.5%), 47 (37.0%), 20 (15.7%), 53 (41.7%) patients with Nestin negative, low, moderate, high expression, respectively. CD133 and Nestin were both correlated with advanced WHO grade but not with age or gender, and positive correlation was observed between CD133 and Nestin. For survival, both CD133 and Nestin were correlated with unfavorable overall survival (OS), and further analysis illustrated that Nestin but not CD133 independently predicted poor OS. Subgroup analysis also revealed that Nestin but not CD133 negatively associated with shorter OS in LGA patients, while both CD133 and Nestin were correlated with poor OS in HGA patients. Conclusion CD133 and Nestin present as potential biomarkers for advanced pathological grade and poor survival in patients with astrocytic tumor.

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Section: Discussionmentioning

confidence: 85%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Clinical significance of CD133 and Nestin in astrocytic tumor: The correlation with pathological grade and survival

Zhang

Chen

et al. 2019

Clinical Laboratory Analysis

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“…The transcription factors hypoxia-inducible factor-1α (HIF-1α) and HIF-2α are highly expressed in niches and in turn upregulate expression of stem cell genes, such as CD133 and sex-determining region Y-box factor 2 (SOX2) for GSCs, and CD133 and CD150 for HSCs [12]. In addition, hypoxia upregulates the expression of SDF-1α and its receptor CXCR4 in glioblastoma tumors and bone marrow via HIF-1α [9,[15][16][17][18][19]. In Figure 1, a peri-arteriolar HSC niche in bone marrow (Figure 1A, B) and a peri-arteriolar GSC niche in a glioblastoma tumor ( Figure 1C, D) are shown.…”

mentioning

confidence: 99%

CXCR4 Antagonists as Stem Cell Mobilizers and Therapy Sensitizers for Acute Myeloid Leukemia and Glioblastoma?

Hira

Noorden

Molenaar

2020

Biology

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Glioblastoma is the most aggressive and malignant primary brain tumor in adults and has a poor patient survival of only 20 months after diagnosis. This poor patient survival is at least partly caused by glioblastoma stem cells (GSCs), which are slowly-dividing and therefore therapy-resistant. GSCs are localized in protective hypoxic peri-arteriolar niches where these aforementioned stemness properties are maintained. We previously showed that hypoxic peri-arteriolar GSC niches in human glioblastoma are functionally similar to hypoxic peri-arteriolar hematopoietic stem cell (HSC) niches in human bone marrow. GSCs and HSCs express the receptor C-X-C receptor type 4 (CXCR4), which binds to the chemoattractant stromal-derived factor-1α (SDF-1α), which is highly expressed in GSC niches in glioblastoma and HSC niches in bone marrow. This receptor-ligand interaction retains the GSCs/HSCs in their niches and thereby maintains their slowly-dividing state. In acute myeloid leukemia (AML), leukemic cells use the SDF-1α-CXCR4 interaction to migrate to HSC niches and become slowly-dividing and therapy-resistant leukemic stem cells (LSCs). In this communication, we aim to elucidate how disruption of the SDF-1α-CXCR4 interaction using the FDA-approved CXCR4 inhibitor plerixafor (AMD3100) may be used to force slowly-dividing cancer stem cells out of their niches in glioblastoma and AML. Ultimately, this strategy aims to induce GSC and LSC differentiation and their sensitization to therapy.

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The role of m6A‐modified CircEPHB4 in glioma pathogenesis: Insights into cancer stemness metastasis

Liao,

Qiu,

Liu

et al. 2023

Ann Clin Transl Neurol

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ObjectiveWhile existing literature has provided insights into involvement of circEPHB4, SOX2 in glioma, their precise molecular mechanisms and synergistic implications in glioma pathogenesis still dim. This study aims to investigate significance and underlying mechanism of m6A‐modified circEPHB4 in regulating SOX2/PHLDB2 axis in gliomas.MethodsThe mRNA and protein expression were tested by qRT‐PCR and Western blot, respectively. ChIP assay was performed to detect SOX2 enrichment on the PHLDB2 promoter. Cell sphere‐forming assay to detect self‐renewal ability, flow cytometry to determine positivity of CD133 expressions, Malignant behavior of glioma cells were detected by CCK‐8, plate colony formation, scratch, and transwell assays. Glioma xenograft models were constructed to investigate effects of CircEPHB4 in tumor development in vivo.ResultsMethyltransferase MELLT3 upregulated m6A modification of CircEPHB4, and YTHDC1 promoted cytoplasmic localization of m6A‐modified CircEPHB4. Overexpression of wild‐type CircEPHB4 enhanced glioma cells' stemness, metastasis, and proliferation. Cytoplasmic CircEPHB4 increased SOX2 mRNA stability by binding to IGF2BP2, and the effects observed by SOX2 knockdown were reversed by CircEPHB4 in glioma cells. SOX2 promoted transcriptional expression of PHLDB2 by enriching the PHLDB2 promoter region. SOX2 reversed the inhibition of PHLDB2 knockdown on stemness of glioma, cell proliferation, and metastasis. In vivo experiments also revealed that CircEPHB4 upregulated PHLDB2 expression by stabilizing SOX2 mRNA, which promoted in vivo tumor growth and accelerated stemness of glioma cells and metastasis.ConclusionThis study reveals functional interaction and molecular mechanisms of m6A‐modified circEPHB4 in regulating SOX2/PHLDB2 axis, highlighting their importance in glioma pathogenesis and potential as therapeutic targets.

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The clinicopathological significance of CD133 and Sox2 in astrocytic glioma

Abstract: Astrocytoma with CD133 and Sox2 overexpression had an unfavorable prognosis and poor clinical response to the current therapeutic protocol.

Cited by 9 publications

References 52 publications

Clinical significance of CD133 and Nestin in astrocytic tumor: The correlation with pathological grade and survival

Clinical significance of CD133 and Nestin in astrocytic tumor: The correlation with pathological grade and survival

CXCR4 Antagonists as Stem Cell Mobilizers and Therapy Sensitizers for Acute Myeloid Leukemia and Glioblastoma?

The role of m6A‐modified CircEPHB4 in glioma pathogenesis: Insights into cancer stemness metastasis

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