Musashi1, an evolutionarily conserved neural RNA-binding protein, is a versatile marker of human glioma cells in determining their cellular origin, malignancy, and proliferative activity

Kanemura, Yonehiro; Yamasaki, Mami; Mori, Kanji; Fujikawa, Hirokazu; Hayashi, Hiroshi; Nakano, Atsuhisa; Matsumoto, Tsuyoshi; Tamura, K; Arita, Norio; Sakakibara, Shin-ichi; Ohnishi, Takanori; Fushiki, Shinji; Nakamura, Yasuhiro; Imai, Toshio; Okano, Hideyuki

doi:10.1046/j.1432-0436.2001.680208.x

Cited by 130 publications

(120 citation statements)

References 40 publications

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“…Our result indicates that P/ musashi1 acts in gliomas in addition to the normal fetal neural progenitor cells. While its activity in terminally differentiated normal tissue was not fully examined, the expression level of Musashi1 is much higher in gliomas than in the surrounding normal brain tissues, 12 indicating the glioma selectivity of the present strategy. However, it should be noted that Musashi1 is also expressed in intestinal epithelial stem cells.…”

Section: Discussionmentioning

confidence: 94%

“…12,13 Firstly, we checked the mRNA expression of Musashi1 in human glioma cell lines and several of the other cancer cell lines by RT-PCR analysis. We confirmed that Musashi1 mRNA expression is restricted to glioma and neuroblastoma cell lines as far as those tested in this study.…”

Section: Discussionmentioning

confidence: 99%

“…[8][9][10][11] Recently, it has been elucidated that Musashi1 is expressed by a variety of tumors, especially malignant gliomas and could be used as a marker for malignant gliomas. 12,13 On the other hand, it was shown that the mouse Musashi1 promoter (P/musashi1) is functional also in the fetal human brain, and neural stem cells can be sorted by fluorescenceactivated cell sorting (FACS) on the basis of P/musashi1-driven green fluorescent protein (GFP) expression. 14 Several strategies were reported to render HSV replication selective for tumor cells: (i) deletion or mutation of viral genes needed for replication in postmitotic cells, [15][16][17] (ii) deletion of the viral genes responsible for regulating viral progeny production, [18][19][20] (iii) use of tumor-specific promoters to regulate the expression of essential viral genes, 21,22 (iv) altering the receptor specificity of HSV glycoproteins toward tumor rather than normal tissue 23 and so on.…”

Section: Introductionmentioning

confidence: 99%

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Enhanced therapeutic efficacy of G207 for the treatment of glioma through Musashi1 promoter retargeting of γ34.5-mediated virulence

et al. 2005

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G207 is a conditionally replicating derivative of herpes simplex virus type1 (HSV-1) engineered with deletions of both ICP34.5 loci and a lacZ insertion disabling the ICP6 gene. G207 exhibits an efficient oncolytic activity in vitro and in vivo, yet minimal toxicity in normal tissue, and is now in clinical trial for malignant glioma. According to the results of clinical trials, however, although G207 was proved to be safe, the efficacy was not so impressive. Deletion of the ICP34.5 gene coding for virulence made G207 extremely safe, but it markedly reduced the cytotoxicity mediated by HSV-1. To enhance the therapeutic efficacy of G207 without diminishing its safety, we used a defective vector containing Musashi1 promoter/ICP34.5, with G207 as helper virus. P/musashi1 was functional selectively in human glioma cell lines (U87MG, U251, T98G) in this study and dvM345 showed a much higher therapeutic efficacy both in culture and in the in vivo glioma model, than G207 alone, without diminishing its favorable toxicity profile. These results suggest that transcriptional regulation of ICP34.5 by P/musashi1 can be used to target HSV-1 virulence toward gliomas while maintaining the desirable neuroattenuated phenotype.

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Section: Discussionmentioning

confidence: 94%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Enhanced therapeutic efficacy of G207 for the treatment of glioma through Musashi1 promoter retargeting of γ34.5-mediated virulence

et al. 2005

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“…Several reports showed higher expression of selective makers of neural stem/progenitor cells, like nestin or musashi1, in malignant gliomas suggesting the biological analogy between neural stem/progenitor cells and glioma cells and the usefulness of these markers for clinical diagnosis of malignant gliomas. 21,28 Present findings suggest D2-40 may be a useful marker for characterizing tumor properties and for examining in situ the analogy between normal neural stem/ D2-40 in brain Y Nakamura et al progenitor cells and brain tumor cells. The result that pineal germinoma was intensely positively stained with D2-40 is reasonable because of positivity in seminoma and dysgerminoma.…”

Section: Discussionmentioning

confidence: 70%

D2-40 antibody immunoreactivity in developing human brain, brain tumors and cultured neural cells

et al. 2006

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D2-40 antibody is raised against an oncofetal antigen, the M2A antigen. It has been used as a marker for lymphatic endothelium as well as mesothelioma and cerebellar hemangioblastoma. We demonstrate here that positive D2-40 immunoreactivity was found in the developing cerebrum, particularly in the germinal matrix layer, immature ependyma, choroid plexus and meninges. In the developing cerebellum, positive D2-40 immunoreactivity was found in the external granular layer particularly of the outer portion and the Purkinje cell layer as well as meninges. Some brain tumors such as anaplastic ependymoma, some medulloblastomas, glioblastoma, pineal germinoma, craniopharyngioma, choroid plexus papilloma, choroid plexus carcinoma, and meningioma showed positive immunoreactivity with D2-40. Therefore, D2-40 antibody is considered a useful marker for research on developing brain and diagnosis of brain tumors, differentiation between choroid plexus carcinoma and metastatic carcinoma. In addition, on cultured human neural cells, D2-40 immunoreactivity was found in nestin-positive neural stem/progenitor cells and neuronal lineage cells. As D2-40 antibody recognizes cell surface antigen M2A, it might be a candidate cell surface marker for isolation of human neural stem cells/ neuronal lineage cells in the fluorescence-activated cell sorting technique.

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“…Y. H. Ma et al [39] demonstrated increase of Musashi-1 in the glioma cells compared with normal tissue and correlation of high expression of mRNA protein with the malignancy degree. A correlation was established between Мusashi-1 expression and proliferative Bmi-1 marker in malignant gliomas [40].…”

Section: Origin Isolation and Phenotypic Characteristicіs Of The Bramentioning

confidence: 99%

Brain tumor stem cells: phenotypic characterization and directed therapeutic approaches

Belska¹,

Lisianyi²

2015

JCOT

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The review presents the current conceptions of the origin, methods of isolation and phenotypic characterization of the brain tumor stem cells. Phenotypic similarity in molecular markers between cancer and neural stem cells is shown. Therapeutic approaches of impact on the brain tumor stem cells and on the intracellular signaling pathways of cancer stem cells are described. KEYWORDS: brain tumor stem cells, neural stem cells, malignant gliomas, CD133, nestinnumber of CSCs in different types of cancer varies from 1 % to 20 % and even more in some cases. The brain tumor stem cells (BTSCs) possess an indefinite capacity for self-maintenance, tumor generation during ortotopic implantation, genetic disorders and formation of cancer cells [6]. BTSCs possess great capacity for invasion, stimulate formation of the blood vessels and initiate cell migration [2,3]. Apart from this, they are involved in the stimulation of cancerogenesis: there appear more and more corroborations that these cells promote cancer progression [7] and metastasis [8]. This type of cells is responsible for chemo-and radio resistance, post-surgery and radiotherapy relapse.

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Musashi1, an evolutionarily conserved neural RNA-binding protein, is a versatile marker of human glioma cells in determining their cellular origin, malignancy, and proliferative activity

Cited by 130 publications

References 40 publications

Enhanced therapeutic efficacy of G207 for the treatment of glioma through Musashi1 promoter retargeting of γ34.5-mediated virulence

Enhanced therapeutic efficacy of G207 for the treatment of glioma through Musashi1 promoter retargeting of γ34.5-mediated virulence

D2-40 antibody immunoreactivity in developing human brain, brain tumors and cultured neural cells

Brain tumor stem cells: phenotypic characterization and directed therapeutic approaches

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