Glioma Initiating Cells Form a Differentiation Niche Via the Induction of Extracellular Matrices and Integrin αV
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{"title"=>"Glioma Initiating Cells Form a Differentiation Niche Via the Induction of Extracellular Matrices and Integrin αV", "type"=>"journal", "authors"=>[{"first_name"=>"Akiko", "last_name"=>"Niibori-Nambu", "scopus_author_id"=>"55981461300"}, {"first_name"=>"Uichi", "last_name"=>"Midorikawa", "scopus_author_id"=>"55694424000"}, {"first_name"=>"Souhei", "last_name"=>"Mizuguchi", "scopus_author_id"=>"7004170485"}, {"first_name"=>"Takuichiro", "last_name"=>"Hide", "scopus_author_id"=>"6701569894"}, {"first_name"=>"Minako", "last_name"=>"Nagai", "scopus_author_id"=>"55734716000"}, {"first_name"=>"Yoshihiro", "last_name"=>"Komohara", "scopus_author_id"=>"22941122600"}, {"first_name"=>"Megumi", "last_name"=>"Nagayama", "scopus_author_id"=>"55693876100"}, {"first_name"=>"Mio", "last_name"=>"Hirayama", "scopus_author_id"=>"55693571000"}, {"first_name"=>"Daiki", "last_name"=>"Kobayashi", "scopus_author_id"=>"55057818800"}, {"first_name"=>"Nobuyuki", "last_name"=>"Tsubota", "scopus_author_id"=>"36904995900"}, {"first_name"=>"Tatsuya", "last_name"=>"Takezaki", "scopus_author_id"=>"25639111000"}, {"first_name"=>"Keishi", "last_name"=>"Makino", "scopus_author_id"=>"7202528239"}, {"first_name"=>"Hideo", "last_name"=>"Nakamura", "scopus_author_id"=>"36080033300"}, {"first_name"=>"Motohiro", "last_name"=>"Takeya", "scopus_author_id"=>"7101872886"}, {"first_name"=>"Junichi", "last_name"=>"Kuratsu", "scopus_author_id"=>"21737319700"}, {"first_name"=>"Norie", "last_name"=>"Araki", "scopus_author_id"=>"55532261700"}], "year"=>2013, "source"=>"PLoS ONE", "identifiers"=>{"sgr"=>"84877964710", "doi"=>"10.1371/journal.pone.0059558", "issn"=>"19326203", "pui"=>"368960630", "isbn"=>"1932-6203 (Electronic)\\r1932-6203 (Linking)", "pmid"=>"23704872", "scopus"=>"2-s2.0-84877964710"}, "id"=>"61963a32-6d14-3474-82aa-d7246410b192", "abstract"=>"Glioma initiating cells (GICs) are considered responsible for the therapeutic resistance and recurrence of malignant glioma. 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Integrin αV blocking antibody and RGD peptide significantly suppressed early events in GIC differentiation, suggesting that the coupling of ECMs to integrin αV is necessary for GIC differentiation. In addition, the expression of integrin αV and its strong ligand FN was prominently increased in glioblastomas developed from mouse intracranial GIC xenografts. Interestingly, during the initial phase of GIC differentiation, the RGD treatment significantly inhibited GIC proliferation and raised their sensitivity against anti-cancer drug temozolomide (TMZ). We also found that combination treatments of TMZ and RGD inhibit glioma progression and lead the longer survival of mouse intracranial GIC xenograft model. These results indicate that GICs induce/secrete ECMs to develop microenvironments with serum factors, namely differentiation niches that further stimulate GIC differentiation and proliferation via the integrin recognition motif RGD. 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To clarify the molecular mechanism of GIC maintenance/differentiation, we established GIC clones having the potential to differentiate into malignant gliomas, and subjected to DNA microarray/iTRAQ based integrated proteomics. 21,857 mRNAs and 8,471 proteins were identified and integrated into a gene/protein expression analysis chart. Gene Ontology analysis revealed that the expression of cell adhesion molecules, including integrin subfamilies, such as <u>α</u>2 and <u>α</u>V, and extracellular matrices (ECMs), such as collagen IV (COL4), laminin <u>α</u>2 (LAMA2), and fibronectin 1 (FN), was significantly upregulated during serum-induced GIC differentiation. This differentiation process, accompanied by the upregulatio<u>n</u> of MAPK as well as glioma specific proteins in GICs, was dramatically accelerated in these ECM (especially FN)-coated dishes. Integrin <u>α</u>V blocking antibody and RGD peptide significantly suppressed early events in GIC differentiation, suggesting that the coupling of ECMs to integrin <u>α</u>V is necessary for GIC differentiation. In addition, the expression of integrin <u>α</u>V and its strong ligand FN was prominently increased in glioblastomas developed from mouse intracranial GIC xenografts. Interestingly, during the initial phase of GIC differentiation, the RGD treatment significantly inhibited GIC proliferation and raised their sensitivity against anti-cancer drug temozolomide (TMZ). We also found that combination treatments of TMZ and RGD inhibit glioma progression and lead the longer survival of mouse intracranial GIC xenograft model. These results indicate that GICs induce/secrete ECMs to develop microenvironments with serum factors, namely differentiation niches that further stimulate GIC differentiation and proliferation via the integrin recognition motif RGD. A combination of RGD treatment with TMZ could have the higher inhibitory potential against the glioma recurrence that may be regulated by the GICs in the differentiation niche. 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Relative Metric

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