Musashi1 modulates cell proliferation genes in the medulloblastoma cell line Daoy

Sánchez-Díaz, Patricia C.; Burton, Tarea; Burns, Suzanne Perea; Hung, Jaclyn Y.; Penalva, Luiz O.

doi:10.1186/1471-2407-8-280

Cited by 68 publications

(91 citation statements)

References 46 publications

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“…28 Silencing of MSI1 in DAOY medulloblastoma cells decreased proliferation and neurosphere formation, and induced differentiation and apoptosis. 29 In the particular case of glioblastoma, we observed that a reduction in MSI1 expression increased apoptosis, decreased proliferation, affected cell cycle regulation, and interfered with adhesion-related functions such as invasion and migration. 13 However, the impact of MSI1 expression on treatment outcome is poorly understood.…”

Section: Discussionmentioning

confidence: 95%

Musashi1 Impacts Radio-Resistance in Glioblastoma by Controlling DNA-Protein Kinase Catalytic Subunit

Araújo

Gorthi

Silva

et al. 2016

The American Journal of Pathology

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The conserved RNA-binding protein Musashi1 (MSI1) has been characterized as a stem cell marker, controlling the balance between self-renewal and differentiation and as a key oncogenic factor in numerous solid tumors, including glioblastoma. To explore the potential use of MSI1 targeting in therapy, we studied MSI1 in the context of radiation sensitivity. Knockdown of MSI1 led to a decrease in cell survival and an increase in DNA damage compared to control in cells treated with ionizing radiation. We subsequently examined mechanisms of double-strand break repair and found that loss of MSI1 reduces the frequency of nonhomologous end-joining. This phenomenon could be attributed to the decreased expression of DNAeprotein kinase catalytic subunit, which we have previously identified as a target of MSI1. Collectively, our results suggest a role for MSI1 in double-strand break repair and that its inhibition may enhance the effect of radiotherapy. Glioblastoma multiforme is the most aggressive form of glioma and is the most common among primary brain tumors. The current standard of care for newly diagnosed glioblastoma is surgical resection, followed by concurrent temozolomide and radiotherapy, then by maintenance chemotherapy with temozolomide. Unfortunately, this route offers a median survival of only approximately 14 months.

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Section: Discussionmentioning

confidence: 95%

Musashi1 Impacts Radio-Resistance in Glioblastoma by Controlling DNA-Protein Kinase Catalytic Subunit

Araújo

Gorthi

Silva

et al. 2016

The American Journal of Pathology

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“…Msi-1 is an RNA binding protein which is preferentially expressed in stem-cells, functions as a translational repressor (56)(57)(58), and is widely used as a molecular marker to identify stem cells in embryos and adult tissues (26)(27)(28)(29). In our study, Msi-1 was expressed in five MRT cell lines except TTC642, which originated from a neck mass.…”

Section: Discussionmentioning

confidence: 93%

“…In recent years, the concept of CSC involvement in tumorigenesis has attracted the attention of many researchers. Previous studies have shown that NSC acting as CSC is recognized in CNS (24)(25)(26)(27)(28)(29). In the present study, we examined the expression of NSC markers such as CD133, nestin and Msi-1 before and after 4-HPR induced differentiation in MRT cell lines to elucidate the cytological characteristics of MRT cells that are considered to derive from neuroectodermal origin (8,9,12).…”

Section: Introductionmentioning

confidence: 99%

Expression of neural stem cell markers in malignant rhabdoid tumor cell lines

Okuno

Ohta²,

Katô³

et al. 2009

Oncol Rep

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Abstract. Malignant rhabdoid tumor (MRT) is considered to display multi-phenotypic characteristics but the true origin of this tumor remains unknown. In recent years, the concept of the cancer stem cell (CSC) has drawn great attention. In the present study we investigated six MRT cell lines (TM87-16, STM91-01, TTC642, TTC549, YAM-RTK-1 and TTC1240), for CD133, nestin and Musashi-1 (Msi-1), which are considered to be CSC as well as neural stem cell (NSC) markers, using assays for cell viability and apoptosis, reverse transcriptional polymerase chain reaction (RT-PCR), semiquantitative PCR and Western blot analysis before and after differentiation-induction with N-(4-hydroxyphenyl) retinamid (4-HPR). Before differentiation-induction with 4-HPR, CD133 was detected in three MRT cell lines, nestin in three cell lines and Msi-1 in five cell lines. In TTC549 after differentiation-induction with 4-HPR, nestin and Msi-1 were down-regulated in a time-dependent manner. Similar downregulation of Msi-1 was recognized in YAM-RTK-1. In STM91-01, CD133 was gradually down-regulated and Msi-1 was down-regulated after a transient increase. Results from our study indicated that 4-HPR might be effective in some MRTs. Expression of NSC markers showed that some MRTs contain a subpopulation of NSC and down-regulation of NSC markers in MRT cells provides supportive evidence that many MRTs could be considered of neuroectodermal origin.

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“…A disease of great relevance to Msi1 is cancer, because many carcinoma cells are of epithelial stem cell lineage (48), expressing Msi1 protein. Strong expression of the Msi1 protein has been observed in many tumors, such as glioma (25), hepatoma (26), colorectal adenoma (27,49), teratoid/rhabdoid tumors in eye (50), non-small cell lung cancer (51), retinoblastoma (52), medulloblastoma (53,54), ependymoma (53), endometrial carcinoma (55), neurocytoma (56), glioblastoma (57), cervical carcinoma (58), etc. Although the exact function of Msi1 in these cancer cells remains unclear, knockdown of Msi1 by using siRNA resulted in tumor growth arrest in colon adenocarcinoma xenografts transplanted in athymic nude mice, reduced cancer cell proliferation, and increased apoptosis (59).…”

Section: Msi1 and Diseasesmentioning

confidence: 99%

Notch Signaling in Hair Follicle Development

Bae¹,

Heon²,

이인호³

et al. 2017

Asian J Beauty Cosmetol

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The Musashi family is an evolutionarily conserved group of RNA-binding proteins. In mammal, two members of the group, Msi1 and Msi2, have been identified to date. Msi1 is considered to play roles in maintaining the stem cell status (stemness) of neural stem/progenitor cells in adults and in the development of central nervous system through translational regulation of its target mRNAs, which encode regulators of signal transduction and the cell cycle. Recently, strong expression of Msi1 in various somatic stem/progenitor cells of adult tissues, such as eye, gut, stomach, breast, and hair follicle, has been reported. The protein is also expressed in various cancer cells, and ectopically emerging cells have been found in neural tissues of patients with diseases involving neural disorder, including epilepsy. Many novel target mRNAs and regulatory pathways of Msi1 have been reported in recent years. Here, we present a review of the functions and action mechanisms of Msi1 protein and discuss possible directions for further study.

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Musashi1 modulates cell proliferation genes in the medulloblastoma cell line Daoy

Abstract: Background: Musashi1 (Msi1) is an RNA binding protein with a central role during nervous system development and stem cell maintenance. High levels of Msi1 have been reported in several malignancies including brain tumors thereby associating Msi1 and cancer.

Cited by 68 publications

References 46 publications

Musashi1 Impacts Radio-Resistance in Glioblastoma by Controlling DNA-Protein Kinase Catalytic Subunit

Musashi1 Impacts Radio-Resistance in Glioblastoma by Controlling DNA-Protein Kinase Catalytic Subunit

Expression of neural stem cell markers in malignant rhabdoid tumor cell lines

Notch Signaling in Hair Follicle Development

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