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dc.contributor.authorCheng, Ru-Binzh_CN
dc.contributor.authorMa, Rui-Juanzh_CN
dc.contributor.authorWang, Zhao-Kaizh_CN
dc.contributor.authorYang, Shan-Junzh_CN
dc.contributor.authorLin, Xiang-Zhizh_CN
dc.contributor.authorRong, Huizh_CN
dc.contributor.authorMa, Yongzh_CN
dc.contributor.author程汝滨zh_CN
dc.date.accessioned2015-07-22T03:12:06Z
dc.date.available2015-07-22T03:12:06Z
dc.date.issued2011-03zh_CN
dc.identifier.citationMOLECULAR AND CELLULAR BIOCHEMISTRY, 2011,349:149-157zh_CN
dc.identifier.otherWOS:000288398300015zh_CN
dc.identifier.urihttps://dspace.xmu.edu.cn/handle/2288/87837
dc.description.abstractCD133 is extensively used as a surface marker to identify and isolate glioma-initiating cells (GICs) from malignant brain tumors; however, instances of CD133(-) cells exhibiting similar properties have also been reported. To clarify the availability of CD133 as the GIC marker, we first evaluated the ratio of CD13(+) cells and malignancy of glioma spheroids GIC1 and GIC2, respectively. GIC1, which showed a lower percentage of CD133(+) cells, exhibited a highly aggressive behavior in comparison with GIC2. The following experiments demonstrated that tumor suppressor PTEN was lost in GIC1, resulting in the activation of AKT pathway. Overexpression of recombinant PTEN in GIC1 suppressed its proliferation and self-renew without significant effect on CD133 expression level, indicating that the inconsistence between the ratio of CD133(+) cells and proliferation and self-renewal capacity of GIC1 and GIC2 was caused by PTEN deficiency. To further validate our conclusion, a series of GICs were analyzed and the percentages of CD133(+) cells could not reflect the degrees of cell proliferation and self-renewal characteristics in the PTEN deficient GICs, suggesting that the application of CD133 as the GIC maker was restricted by PTEN loss. Furthermore, down-regulation of PTEN in the PTEN-expressing GICs could break the positive correlation between the ratio of CD133(+) cells and proliferation and self-renewal capacity. Our results demonstrated that PTEN status is related to cell proliferation and self-renewal independent of CD133 phenotype in the glioma-initiating cells, resulting in the limitations of CD133 as a biomarker for PTEN deficient GICs.zh_CN
dc.language.isoen_USzh_CN
dc.publisherMOL CELL BIOCHEMzh_CN
dc.source.urihttp://dx.doi.org/10.1007/s11010-010-0669-1zh_CN
dc.subjectCANCER STEM-CELLzh_CN
dc.subjectBRAIN-TUMORSzh_CN
dc.subjectMALIGNANT GLIOMASzh_CN
dc.subjectMARKER CD133zh_CN
dc.subjectIN-VIVOzh_CN
dc.subjectGLIOBLASTOMAzh_CN
dc.subjectIDENTIFICATIONzh_CN
dc.subjectRESISTANCEzh_CN
dc.subjectSUPPRESSORzh_CN
dc.subjectEXPRESSIONzh_CN
dc.titlePTEN status is related to cell proliferation and self-renewal independent of CD133 phenotype in the glioma-initiating cellszh_CN
dc.typeArticlezh_CN


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