Fatty acid binding protein 7 as a marker of glioma stem cells

Morihiro, Yusuke; Yasumoto, Yuki; Vaidyan, Linda Koshy; Sadahiro, Hirokazu; Uchida, Tatsuo; Inamura, Akinori; Sharifi, Kazem; Ideguchi, Makoto; Nomura, Sadahiro; Tokuda, Nobuko; Kashiwabara, Shoji; Ishii, Aya; Ikeda, Eiji; Owada, Yuji; Suzuki, Michiyasu

doi:10.1111/pin.12109

Cited by 38 publications

(43 citation statements)

References 36 publications

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“…More recently, FABP7 has been recognized as a NOTCH1 target with a key role in the maintenance of radial glia cells with NSC properties . Interestingly, FABP7 is a shared NOTCH1/SOX10 target that marks neural stem cells in the subventricular CNS zone, as well as CSC in glioblastoma . Fatty acid‐binding protein 7 is coexpressed with SOX10 in ACC and basal‐like breast cancers, and in these tumor types FABP7 expression serves as a diagnostic marker associated with poor prognosis .…”

Section: Resultsmentioning

confidence: 99%

“…[136][137][138][139][140] Interestingly, FABP7 is a shared NOTCH1/SOX10 target 136,141 that marks neural stem cells in the subventricular CNS zone, as well as CSC in glioblastoma. [142][143][144] Fatty acidbinding protein 7 is coexpressed with SOX10 in ACC and basal-like breast cancers, 97 and in these tumor types FABP7 expression serves as a diagnostic marker associated with poor prognosis. 79,145 Although the mechanism of FABP7 activity in cancer or CSC maintenance is not well described, activation of FABP7 in cancers increases fatty acid uptake resulting in enhanced cell survival and protection against reactive oxygen species.…”

Section: Fatty Acid-binding Proteinmentioning

confidence: 99%

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Clinical and molecular insights into adenoid cystic carcinoma: Neural crest‐like stemness as a target

Yarbrough

Panaccione

Chang

et al. 2016

Laryngoscope Investig Oto

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ObjectivesThis review surveys trialed therapies and molecular defects in adenoid cystic carcinoma (ACC), with an emphasis on neural crest‐like stemness characteristics of newly discovered cancer stem cells (CSCs) and therapies that may target these CSCs.Data SourcesArticles available on Pubmed or OVID MEDLINE databases and unpublished data.Review MethodsSystematic review of articles pertaining to ACC and neural crest‐like stem cells.ResultsAdenoid cystic carcinoma of the salivary gland is a slowly growing but relentless cancer that is prone to nerve invasion and metastases. A lack of understanding of molecular etiology and absence of targetable drivers has limited therapy for patients with ACC to surgery and radiation. Currently, no curative treatments are available for patients with metastatic disease, which highlights the need for effective new therapies. Research in this area has been inhibited by the lack of validated cell lines and a paucity of clinically useful markers. The ACC research environment has recently improved, thanks to the introduction of novel tools, technologies, approaches, and models. Improved understanding of ACC suggests that neural crest‐like stemness is a major target in this rare tumor. New cell culture techniques and patient‐derived xenografts provide tools for preclinical testing.ConclusionPreclinical research has not identified effective targets in ACC, as confirmed by the large number of failed clinical trials. New molecular data suggest that drivers of neural crest‐like stemness may be required for maintenance of ACC; as such, CSCs are a target for therapy of ACC.

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Section: Resultsmentioning

confidence: 99%

Section: Fatty Acid-binding Proteinmentioning

confidence: 99%

Clinical and molecular insights into adenoid cystic carcinoma: Neural crest‐like stemness as a target

Yarbrough

Panaccione

Chang

et al. 2016

Laryngoscope Investig Oto

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“…Within the central cell cluster, a subset of cells expresses other stem cell-associated genes, such as isl1 and fabp7a (clusters 7, 9; Fig. 1K; (Kim et al, 2016;Makarev and Gorivodsky, 2014;Morihiro et al, 2013;Shin et al, 2007)). In addition, members of the retinoic acid pathway, such as crabp2a, dhrs3a and rdh10a are restricted to clusters 7 and 9 ( Fig.…”

Section: Single Cell Rna-seq Reveals Support Cell Heterogeneitymentioning

confidence: 99%

Single cell RNA-Seq reveals distinct stem cell populations that drive sensory hair cell regeneration in response to loss of Fgf and Notch signaling

Koenecke

et al. 2018

Preprint

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Loss of sensory hair cells leads to deafness and balance deficiencies. In contrast to mammalian hair cells, zebrafish ear and lateral line hair cells regenerate from poorly characterized, proliferating support cells. Equally ill-defined is the gene regulatory network underlying the progression of support cells to cycling hair cell progenitors and differentiated hair cells. We used single cell RNA-Sequencing (scRNA-Seq) of lateral line sensory organs and uncovered five different support cell types, including quiescent and activated stem cells. In silico ordering of support cells along a developmental trajectory identified cells that self-renew and new groups of genes required for hair cell differentiation. scRNA-Seq analyses of fgf3 mutants, in which hair cell regeneration is increased, demonstrates that Fgf and Notch signaling inhibit proliferation of support cells in parallel by inhibiting Wnt signaling. Our scRNA-Seq analyses set the foundation for mechanistic studies of sensory organ regeneration and is crucial for identifying factors to trigger hair cell production in mammals. As a resource, we implemented a shiny application that allows the community to interrogate cell type specific expression of genes of interest.

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“…Most kinds of cancers contain a subset cells which have an indefinite self-renewal potential and could differentiate multidirectional, those cells are called cancer stem cells (CSCs) [2]. Some recent studies reported that the CSCs in gioblastoma (GSCs) had been isolated and identified successfully [3,4].…”

Section: Introductionmentioning

confidence: 99%

MiR-21 up-regulation mediates glioblastoma cancer stem cells apoptosis and proliferation by targeting FASLG

et al. 2014

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To investigate whether miR-21 can affect the apoptosis and proliferation of glioblastoma cancer stem cells (GSCs) from down-regulating FASLG. The expression of miRNA-21 was detected by quantitative real-time PCR in normal brain tissue and glioblastoma samples, and the changes of miRNA-21 expression between GSCs and non-GSCs were also detected. The apoptosis and proliferation ability of miR-21 in GSCs were analyzed by MTT and flow cytometry assay after anti-miR-21 transfection. For the regulation mechanism analysis of miR-21, TargetScan, PicTar and microRNA were selected to predict some potential target genes of miR-21. The predicted gene was identified to be the direct and specific target gene of miR-21 by luciferase activities assay and western blot. RNA interference technology was used to confirm the apoptosis and proliferation effects of miR-21 were directly induced by FASLG. The expression of miR-21 increased significantly in glioblastoma contrast to normal brain tissue, and miR-21 up-regulated in GSCs remarkably. The proliferation of GSCs cell could be inhibited with high-expression of miR-21 and this effect could be restored by miR-21 knocked down. Mechanism analysis revealed that FASLG was a specific and direct target gene of miR-21. The advanced effects of anti-miR-21 on GSCs apoptosis and proliferation were mediated by expression of silenced FASLG. In summary, aberrantly expressed miR-21 regulates GSCs apoptosis and proliferation partly through directly down-regulating FASLG protein expression in GSCs and this might offer a new potential therapeutic stratagem for glioblastoma.

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Fatty acid binding protein 7 as a marker of glioma stem cells

Cited by 38 publications

References 36 publications

Clinical and molecular insights into adenoid cystic carcinoma: Neural crest‐like stemness as a target

Clinical and molecular insights into adenoid cystic carcinoma: Neural crest‐like stemness as a target

Single cell RNA-Seq reveals distinct stem cell populations that drive sensory hair cell regeneration in response to loss of Fgf and Notch signaling

MiR-21 up-regulation mediates glioblastoma cancer stem cells apoptosis and proliferation by targeting FASLG

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