Transforming growth factor-β-inducible gene-h3 (βig-h3) promotes cell adhesion of human astrocytoma cells in vitro: implication of α6β4 integrin

Kim, Miok; Yun, Su Jin; Kim, In San; Sohn, Seonghyang; Lee, Eunjoo H.

doi:10.1016/s0304-3940(02)01260-0

Cited by 56 publications

(46 citation statements)

References 18 publications

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“…These results are corroborated by the observation that the interaction between astrocytoma cells and big-h3, a protein homologue of periostin, is dependent on a 6 b 4 integrin (Kim et al, 2003). Previous studies reported that the a v b 3 and a v b 5 integrin complexes act as the receptors for periostin in breast, colon and ovarian cancer as well as endothelial cells (Gillan et al, 2002;Bao et al, 2004;Shao et al, 2004).…”

Section: Discussionsupporting

confidence: 54%

Periostin promotes invasiveness and resistance of pancreatic cancer cells to hypoxia-induced cell death: role of the β4 integrin and the PI3k pathway

Baril¹,

Gangeswaran²,

Mahon³

et al. 2006

Oncogene

256

244

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Pancreatic ductal adenocarcinoma is a devastating disease, characterized by a rapid progression and poor treatment response. Using gene expression profiling of pancreatic cancer tissues, we previously identified periostin as a potential diagnostic and therapeutic target. In this study, we report the overexpression of periostin in a larger set of pancreatic cancer tissues and show that although the periostin transcript is exclusively expressed in tumour cells, the protein product is only detected in the extracellular matrix adjacent to cancer cells. Using an enzyme-linked immunosorbent assay (ELISA) assay, we show significantly increased levels of periostin in the sera of pancreatic cancer patients compared to non-cancer controls. We demonstrate that periostin promotes the invasiveness of tumour cells by increasing the motility of cells without inducing expression of proteases, and enhances the survival of tumour cells exposed to hypoxic conditions. At the molecular level, we provide evidence that the a 6 b 4 integrin complex acts as the cell receptor of periostin in pancreatic cancer cells and that interaction promotes phosphorylation of focal adhesion kinase (FAK) and protein kinase B (AKT) though activation of the PI3 kinase pathway, but not the RAS/MEK/ERK pathway. These findings suggest an important role of periostin in pancreatic cancer and provide a rationale to study periostin for diagnostic and therapeutic applications.

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Section: Discussionsupporting

confidence: 54%

Periostin promotes invasiveness and resistance of pancreatic cancer cells to hypoxia-induced cell death: role of the β4 integrin and the PI3k pathway

Baril¹,

Gangeswaran²,

Mahon³

et al. 2006

Oncogene

256

244

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“…The secreted CCN gene family members CYR61 and CTGF, which can act as ligands for integrins and stimulate adhesion and migration, are overexpressed in glioma cells and prognostic for tumor progression and survival of glioma patients (19,28). The SPARC-induced secretory protein TGFBI interacts with FN1 (73) and distinct integrins (74,75) and promotes integrin-dependent adhesion of glioblastoma cells (20,76). The integrin-associated protein CD47 serves as a ligand for signal regulatory protein a in malignant glioma cells and is frequently expressed in glioblastomas (77).…”

Section: Discussionmentioning

confidence: 99%

Functional Network Analysis Reveals Extended Gliomagenesis Pathway Maps and Three Novel MYC-Interacting Genes in Human Gliomas

et al. 2005

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Gene expression profiling has proven useful in subclassification and outcome prognostication for human glial brain tumors. The analysis of biological significance of the hundreds or thousands of alterations in gene expression found in genomic profiling remains a major challenge. Moreover, it is increasingly evident that genes do not act as individual units but collaborate in overlapping networks, the deregulation of which is a hallmark of cancer. Thus, we have here applied refined network knowledge to the analysis of key functions and pathways associated with gliomagenesis in a set of 50 human gliomas of various histogenesis, using cDNA microarrays, inferential and descriptive statistics, and dynamic mapping of gene expression data into a functional annotation database. Highest-significance networks were assembled around the myc oncogene in gliomagenesis and around the integrin signaling pathway in the glioblastoma subtype, which is paradigmatic for its strong migratory and invasive behavior. Three novel MYC-interacting genes (UBE2C, EMP1, and FBXW7) with cancer-related functions were identified as network constituents differentially expressed in gliomas, as was CD151 as a new component of a network that mediates glioblastoma cell invasion. Complementary, unsupervised relevance network analysis showed a conserved selforganization of modules of interconnected genes with functions in cell cycle regulation in human gliomas. This approach has extended existing knowledge about the organizational pattern of gene expression in human gliomas and identified potential novel targets for future therapeutic development.

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“…Two of the three nonredundant genes were neuroprotective (Tables S3 and S4): the gene for the antibacterial enzyme lysozyme (Lyz) and the gene for chitinase 3-like 3 (Chi3l3; also known as Ym1) that is characteristically expressed by alternatively activated macrophages, by resting microglia, and at higher levels by alternatively activated microglia (17). The third gene, TGF␤-induced protein (Tgfbi), may also protect against tissue injury because it was induced after a cerebral stab wound in the rat (20).…”

Section: Injection Of Hmscs Suppressed Neurologic Deficits and Neuronalmentioning

confidence: 99%

Stem/progenitor cells from bone marrow decrease neuronal death in global ischemia by modulation of inflammatory/immune responses

Ohtaki

Ylöstalo

Foraker

et al. 2008

Proc. Natl. Acad. Sci. U.S.A.

368

297

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Human mesenchymal stromal cells (hMSCs) were injected into the hippocampus of adult mice 1 day after transient global ischemia. The hMSCs both improved neurologic function and markedly decreased neuronal cell death of the hippocampus. Microarray assays indicated that ischemia up-regulated 586 mouse genes. The hMSCs persisted for <7 days, but they down-regulated >10% of the ischemia-induced genes, most of which were involved in inflammatory and immune responses. The hMSCs also upregulated three mouse genes, including the neuroprotective gene Ym1 that is expressed by activated microglia/macrophages. In addition, the transcriptomes of the hMSC changed with upregulation of 170 human genes and down-regulation of 54 human genes. Protein assays of the hippocampus demonstrated increased expression in microglia/macrophages of Ym1, the cell survival factor insulin-like growth factor 1, galectin-3, cytokines reflective of a type 2 T cell immune bias, and the major histocompatibility complex II. The observed beneficial effects of hMSCs were largely explained by their modulation of inflammatory and immune responses, apparently by alternative activation of microglia and/or macrophages.inflammation ͉ mesenchymal stromal cells ͉ microglia ͉ mesenchymal stem cells O bservations in rodent and primate models suggest that a potential therapy for ischemia of the central nervous system is the administration of the adult stem/progenitor cells from bone marrow referred to as mesenchymal stem cells or multipotent mesenchymal stromal cells (MSCs) (1-3). Administration of MSCs also produced beneficial effects in animal models for neurodegenerative diseases, such as Parkinson's disease, experimental autoimmune encephalomyelitis, and amyotrophic lateral sclerosis (2-5). MSCs initially attracted interest for their ability to differentiate into multiple cellular phenotypes in culture and in vivo (1-7). However, recent observations indicate that only small numbers of the cells engraft into most injured tissues, and they disappear quickly (2-5, 8-10). When human MSCs (hMSCs) were injected into the dentate gyrus (DG) of the hippocampus in adult immunodeficient (ID) mice, most of the cells disappeared within 1 week, but they enhanced proliferation, migration, and neural differentiation of the endogenous neural stem cells (8). These and related observations have focused attention on the paracrine effects of MSCs (2, 3, 11). However, it has not been established whether the beneficial effects of MSCs in ischemic models of brain injury are explained by enhanced neurogenesis (8) or by neuroprotection.Experiments here were performed in a mouse model of global ischemia to assess the neuroprotective effects of hMSCs. Administration of hMSCs 1 day after transient common carotid artery occlusion (tCCAO) improved neurologic function and decreased the delayed neuronal cell death of the hippocampus. Surveys with microarrays indicated that the hMSCs decreased expression of many of the mouse genes that were induced by ischemia and that were involved in inflamma...

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Transforming growth factor-β-inducible gene-h3 (βig-h3) promotes cell adhesion of human astrocytoma cells in vitro: implication of α6β4 integrin

Cited by 56 publications

References 18 publications

Periostin promotes invasiveness and resistance of pancreatic cancer cells to hypoxia-induced cell death: role of the β4 integrin and the PI3k pathway

Periostin promotes invasiveness and resistance of pancreatic cancer cells to hypoxia-induced cell death: role of the β4 integrin and the PI3k pathway

Functional Network Analysis Reveals Extended Gliomagenesis Pathway Maps and Three Novel MYC-Interacting Genes in Human Gliomas

Stem/progenitor cells from bone marrow decrease neuronal death in global ischemia by modulation of inflammatory/immune responses

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