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  1. Article: The S100P/RAGE signaling pathway regulates expression of microRNA-21 in colon cancer cells

    Mercado-Pimentel, Melania E / Benjamin C. Onyeagucha / Qing Li / Angel C. Pimentel / Jana Jandova / Mark A. Nelson

    Federation of European Biochemical Societies FEBS letters. 2015 Aug. 19, v. 589, no. 18

    2015  

    Abstract: S100P signaling through the receptor for advanced glycation end-products (RAGE) contributes to colon cancer invasion and metastasis, but the mechanistic features of this process are obscure. Here, we investigate whether activation of S100P/RAGE signaling ...

    Abstract S100P signaling through the receptor for advanced glycation end-products (RAGE) contributes to colon cancer invasion and metastasis, but the mechanistic features of this process are obscure. Here, we investigate whether activation of S100P/RAGE signaling regulates oncogenic microRNA-21 (miR-21). We show that exogenous S100P up-regulates miR-21 levels in human colon cancer cells, whereas knockdown of S100P results in a decrease of miR-21. Furthermore, blockage of RAGE with anti-RAGE antibody suppresses S100P induction of miR-21. In addition, we found that S100P induction of miR-21 expression involves ERK and is suppressed by the MEK inhibitor U0126. Also, S100P treatment stimulates the enrichment of c-Fos, and AP-1 family members, at the miR-21 gene promoter.
    Keywords advanced glycation end products ; antibodies ; colorectal neoplasms ; genes ; humans ; metastasis ; mitogen-activated protein kinase ; neoplasm cells ; signal transduction
    Language English
    Dates of publication 2015-0819
    Size p. 2388-2393.
    Publishing place Elsevier B.V.
    Document type Article
    ZDB-ID 212746-5
    ISSN 1873-3468 ; 0014-5793
    ISSN (online) 1873-3468
    ISSN 0014-5793
    DOI 10.1016/j.febslet.2015.07.010
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  2. Article ; Online: The S100P/RAGE signaling pathway regulates expression of microRNA-21 in colon cancer cells.

    Mercado-Pimentel, Melania E / Onyeagucha, Benjamin C / Li, Qing / Pimentel, Angel C / Jandova, Jana / Nelson, Mark A

    FEBS letters

    2015  Volume 589, Issue 18, Page(s) 2388–2393

    Abstract: S100P signaling through the receptor for advanced glycation end-products (RAGE) contributes to colon cancer invasion and metastasis, but the mechanistic features of this process are obscure. Here, we investigate whether activation of S100P/RAGE signaling ...

    Abstract S100P signaling through the receptor for advanced glycation end-products (RAGE) contributes to colon cancer invasion and metastasis, but the mechanistic features of this process are obscure. Here, we investigate whether activation of S100P/RAGE signaling regulates oncogenic microRNA-21 (miR-21). We show that exogenous S100P up-regulates miR-21 levels in human colon cancer cells, whereas knockdown of S100P results in a decrease of miR-21. Furthermore, blockage of RAGE with anti-RAGE antibody suppresses S100P induction of miR-21. In addition, we found that S100P induction of miR-21 expression involves ERK and is suppressed by the MEK inhibitor U0126. Also, S100P treatment stimulates the enrichment of c-Fos, and AP-1 family members, at the miR-21 gene promoter.
    MeSH term(s) Calcium-Binding Proteins/metabolism ; Cell Line, Tumor ; Colonic Neoplasms/pathology ; Databases, Genetic ; GPI-Linked Proteins/metabolism ; Gene Expression Regulation, Neoplastic ; Humans ; MicroRNAs/genetics ; Neoplasm Proteins/metabolism ; Promoter Regions, Genetic/genetics ; Receptor for Advanced Glycation End Products ; Receptors, Immunologic/metabolism ; Signal Transduction ; Transcription Factor AP-1/metabolism ; Transcription, Genetic ; Up-Regulation
    Chemical Substances Calcium-Binding Proteins ; GPI-Linked Proteins ; MIRN21 microRNA, human ; MicroRNAs ; Neoplasm Proteins ; RECK protein, human ; Receptor for Advanced Glycation End Products ; Receptors, Immunologic ; S100P protein, human ; Transcription Factor AP-1
    Language English
    Publishing date 2015-07-17
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 212746-5
    ISSN 1873-3468 ; 0014-5793
    ISSN (online) 1873-3468
    ISSN 0014-5793
    DOI 10.1016/j.febslet.2015.07.010
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  3. Article ; Online: S100P/RAGE signaling regulates microRNA-155 expression via AP-1 activation in colon cancer.

    Onyeagucha, Benjamin Chidi / Mercado-Pimentel, Melania E / Hutchison, Jennifer / Flemington, Erik K / Nelson, Mark A

    Experimental cell research

    2013  Volume 319, Issue 13, Page(s) 2081–2090

    Abstract: Accumulating evidence indicates that elevated S100P promotes the pathogenesis of cancers, including colon cancer. S100P exerts its effects by binding to and activating the Receptor for Advance Glycation End-products (RAGE). The effects of up-regulated ... ...

    Abstract Accumulating evidence indicates that elevated S100P promotes the pathogenesis of cancers, including colon cancer. S100P exerts its effects by binding to and activating the Receptor for Advance Glycation End-products (RAGE). The effects of up-regulated S100P/RAGE signaling on cell functions are well documented. Despite these observations, little is known about the downstream targets of S100P/RAGE signaling. In the present study, we demonstrated for the first time that activation of RAGE by S100P regulates oncogenic microRNA-155 (miR-155) expression through Activator Protein-1 (AP-1) stimulation in colon cancer cells. Ectopic S100P up-regulated miR-155 levels in human colon cancer cells. Conversely, knockdown of S100P resulted in a decrease in miR-155 levels. Exogenous S100P induced miR-155 expression, but blockage of the RAGE with anti-RAGE antibody suppressed the induction of miR-155 by exogenous S100P. Attenuation of AP-1 activation through pharmacological inhibition of MEK activation or genetic inhibition of c-Jun activation using dominant negative c-Jun (TAM67) suppressed miR-155 induction by exogenous S100P. Also, S100P treatment stimulated the enrichment of c-Fos, an AP-1 family member, at the miR-155 host gene promoter site. Finally, a functional study demonstrated that miR-155 knockdown decreases colon cancer cell growth, motility, and invasion. Altogether, these data demonstrate that the expression of miR-155 is regulated by S100P and is dependent on RAGE activation and stimulation of AP-1.
    MeSH term(s) Calcium-Binding Proteins/genetics ; Calcium-Binding Proteins/metabolism ; Calcium-Binding Proteins/physiology ; Colonic Neoplasms/genetics ; Colonic Neoplasms/metabolism ; Colonic Neoplasms/pathology ; Gene Expression Regulation, Neoplastic ; Gene Knockdown Techniques ; HEK293 Cells ; Humans ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Models, Biological ; Neoplasm Proteins/genetics ; Neoplasm Proteins/metabolism ; Neoplasm Proteins/physiology ; Receptor for Advanced Glycation End Products ; Receptors, Immunologic/genetics ; Receptors, Immunologic/metabolism ; Receptors, Immunologic/physiology ; Signal Transduction/genetics ; Signal Transduction/physiology ; Transcription Factor AP-1/metabolism ; Transcriptional Activation ; Tumor Cells, Cultured
    Chemical Substances Calcium-Binding Proteins ; MIRN155 microRNA, human ; MicroRNAs ; Neoplasm Proteins ; Receptor for Advanced Glycation End Products ; Receptors, Immunologic ; S100P protein, human ; Transcription Factor AP-1
    Language English
    Publishing date 2013-05-18
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 1493-x
    ISSN 1090-2422 ; 0014-4827
    ISSN (online) 1090-2422
    ISSN 0014-4827
    DOI 10.1016/j.yexcr.2013.05.009
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  4. Article ; Online: Multiple transforming growth factor-beta isoforms and receptors function during epithelial-mesenchymal cell transformation in the embryonic heart.

    Mercado-Pimentel, Melania E / Runyan, Raymond B

    Cells, tissues, organs

    2007  Volume 185, Issue 1-3, Page(s) 146–156

    Abstract: Epithelial-mesenchymal cell transformation (EMT) is a critical process during development of the heart valves. Transition of endothelial cells into mesenchymal cells in the atrioventricular (AV) canal and the outflow tract regions of the heart form the ... ...

    Abstract Epithelial-mesenchymal cell transformation (EMT) is a critical process during development of the heart valves. Transition of endothelial cells into mesenchymal cells in the atrioventricular (AV) canal and the outflow tract regions of the heart form the cardiac cushions that eventually form the heart valves. Collagen gel invasion assay has aided in the identification of molecules that regulate EMT. Among those, transforming growth factor-beta (TGF-beta) ligands and receptors demonstrate a critical role during EMT. In the chick, TGF-beta ligands and some receptors have specific functions during EMT. TGF-beta2 mediates endothelial cell-cell activation and separation, and TGF-beta3 mediates cell invasion into the extracellular matrix. Receptors involved in the EMT process include TGF-beta receptor type II (TBRII), TBRIII, endoglin and the TBRI receptors, ALK2 and ALK5. In contrast, in the mouse model, TGF-beta2 is the only ligand involved in EMT. The TGF-beta2 null mouse has either increased EMT or a mesenchymal cell proliferation after EMT. However, functional studies of TGF-beta1 in vivo and in vitro showed that TGF-beta1 functions in the EMT of the mouse AV canal. Latent TGF-beta-binding protein (LTBP-1) and endoglin have a role in the EMT process. Therefore, TGF-betas mediate cardiac EMT in both embryonic species. Further studies will reveal the identification of ligand and receptor-specific activities.
    MeSH term(s) Activin Receptors, Type I/genetics ; Activin Receptors, Type I/metabolism ; Animals ; Chick Embryo ; Epithelial Cells/cytology ; Mesoderm/cytology ; Models, Biological ; Myocardium/cytology ; Protein Isoforms/genetics ; Protein Isoforms/metabolism ; Protein-Serine-Threonine Kinases ; Receptors, Transforming Growth Factor beta/genetics ; Receptors, Transforming Growth Factor beta/metabolism ; Transforming Growth Factor beta/metabolism
    Chemical Substances Protein Isoforms ; Receptors, Transforming Growth Factor beta ; Transforming Growth Factor beta ; TGF-beta type I receptor (EC 2.7.1.11) ; Protein-Serine-Threonine Kinases (EC 2.7.11.1) ; Activin Receptors, Type I (EC 2.7.11.30) ; transforming growth factor-beta type II receptor (EC 2.7.11.30)
    Language English
    Publishing date 2007
    Publishing country Switzerland
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 1468141-9
    ISSN 1422-6421 ; 1422-6405
    ISSN (online) 1422-6421
    ISSN 1422-6405
    DOI 10.1159/000101315
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  5. Article: Endoglin and Alk5 regulate epithelial-mesenchymal transformation during cardiac valve formation.

    Mercado-Pimentel, Melania E / Hubbard, Antony D / Runyan, Raymond B

    Developmental biology

    2007  Volume 304, Issue 1, Page(s) 420–432

    Abstract: Endoglin is an accessory receptor for TGFbeta and can associate with Alk5 or Alk2. Although prior studies indicated that endoglin and Alk5 were not directly involved in epithelial-mesenchymal transformation (EMT) in the heart, the expression pattern of ... ...

    Abstract Endoglin is an accessory receptor for TGFbeta and can associate with Alk5 or Alk2. Although prior studies indicated that endoglin and Alk5 were not directly involved in epithelial-mesenchymal transformation (EMT) in the heart, the expression pattern of endoglin prompted a re-examination. We here show that loss of endoglin expression mediated by either antisense DNA or siRNA results in a direct perturbation of EMT and reduced expression of EMT markers including slug, runx2, RhoA, and latrophilin-2. An examination of BrdU incorporation shows that, while endoglin regulates proliferation at an early stage, reduced endothelial cell proliferation does not account for the loss of mesenchyme. As Alk5 interacts with endoglin, we utilized siRNA and a specific inhibitor, HTS466284 (HTS), to perturb this receptor as well. Alk5 inhibition produced similar effects to the inhibition of endoglin. There was a reduction in mesenchymal cell formation and loss of EMT marker expression similar to that seen with endoglin. Alk5 kinase inhibition produced a similar loss of EMT marker expression but showed a contrasting upregulation of the proliferation and remodeling markers, Cyclin B2 and beta-catenin. Alk5 and endoglin both mediate endothelial cell proliferation in younger explants but, by stage 16, loss of endoglin no longer alters proliferation rates. These data show that both Alk5 and endoglin are directly involved in the process of EMT, that they interact with both TGFbeta-regulated activation and invasion pathways and that the roles of these receptors change during cardiac development.
    MeSH term(s) Animals ; Bromodeoxyuridine ; Cell Differentiation/physiology ; Chick Embryo ; DNA Primers ; Epithelial Cells/cytology ; Gene Expression Regulation, Developmental/physiology ; Heart Valves/embryology ; In Situ Hybridization ; Mesoderm/cytology ; RNA, Small Interfering/genetics ; Receptors, Transforming Growth Factor beta/metabolism ; Reverse Transcriptase Polymerase Chain Reaction
    Chemical Substances DNA Primers ; RNA, Small Interfering ; Receptors, Transforming Growth Factor beta ; Bromodeoxyuridine (G34N38R2N1)
    Language English
    Publishing date 2007-04-01
    Publishing country United States
    Document type Comparative Study ; Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 1114-9
    ISSN 1095-564X ; 0012-1606
    ISSN (online) 1095-564X
    ISSN 0012-1606
    DOI 10.1016/j.ydbio.2006.12.038
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  6. Article ; Online: MicroRNA-101 (miR-101) post-transcriptionally regulates the expression of EP4 receptor in colon cancers.

    Chandramouli, Anupama / Onyeagucha, Benjamin Chidi / Mercado-Pimentel, Melania E / Stankova, Lenka / Shahin, Nisreen Abu / LaFleur, Bonnie J / Heimark, Ronald L / Bhattacharyya, Achyut K / Nelson, Mark A

    Cancer biology & therapy

    2012  Volume 13, Issue 3, Page(s) 175–183

    Abstract: ... i.e. 15 adenocarcinomas and 9 adenomas) and 16 normal colon specimens for EP4 receptor expression ...

    Abstract Purpose: Expression of the PGE2 receptor, EP4, is up-regulated during colorectal carcinogenesis. However the mechanism leading to deregulation of the EP4 receptor is not known. The present study was conducted to investigate the regulation of EP4 receptor by miRNAs.
    Experimental design: We analyzed 26 colon cancers (i.e. 15 adenocarcinomas and 9 adenomas) and 16 normal colon specimens for EP4 receptor expression by immunohistochemistry. A bioinformatics approached identified putative microRNA binding sites with the 3'-UTR of the EP4 receptor. Both colon cancer cell lines and tumor specimens were analyzed for miR-101 and EP4 expression by qRT-PCR and Western analysis respectively and simultaneously in situ hybridizations was used to confirm our results. In vitro and in vivo assays were used to confirm our clinical findings.
    Results: We observed an inverse correlation between the levels of miR-101 and EP4 receptor protein. Transfection of LS174T cells with miR-101 significantly suppressed a luciferase reporter containing the EP4 receptor-3'-UTR. In contrast, a mutant EP4 receptor-3'-UTR construct was unaffected. Ectopic expression of miR-101 markedly reduced cell proliferation and motility. Co-transfection of EP4 receptor could rescue colon cancer cells from the tumor suppressive effects of miR-101. Moreover, the pharmacologic inhibition of EP4 receptor signaling or silencing of EP4 receptor phenocopied the effect of miR-101. This is the first study to show that the EP4 receptor is negatively regulated by miR-101.
    Conclusions: These data provide new insights in the modulation of EP-4 receptor expression at the post-transcriptional level by miR-101 and suggests therapeutic strategies against miR-101 targets may be warranted.
    MeSH term(s) 3' Untranslated Regions ; Adenocarcinoma/genetics ; Adenocarcinoma/metabolism ; Adenocarcinoma/pathology ; Adenoma/genetics ; Adenoma/metabolism ; Adenoma/pathology ; Base Sequence ; Case-Control Studies ; Cell Line, Tumor ; Cell Movement ; Colonic Neoplasms/genetics ; Colonic Neoplasms/metabolism ; Colonic Neoplasms/pathology ; Gene Expression Regulation, Neoplastic ; Genes, Reporter ; Humans ; Luciferases, Renilla/biosynthesis ; Luciferases, Renilla/genetics ; MicroRNAs/metabolism ; MicroRNAs/physiology ; RNA Interference ; Receptors, Prostaglandin E, EP2 Subtype/genetics ; Receptors, Prostaglandin E, EP2 Subtype/metabolism ; Receptors, Prostaglandin E, EP4 Subtype/genetics ; Receptors, Prostaglandin E, EP4 Subtype/metabolism
    Chemical Substances 3' Untranslated Regions ; MIRN101 microRNA, human ; MicroRNAs ; Receptors, Prostaglandin E, EP2 Subtype ; Receptors, Prostaglandin E, EP4 Subtype ; Luciferases, Renilla (EC 1.13.12.5)
    Language English
    Publishing date 2012-02-21
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 2146305-0
    ISSN 1555-8576 ; 1538-4047
    ISSN (online) 1555-8576
    ISSN 1538-4047
    DOI 10.4161/cbt.13.3.18874
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    Zs.A 5887: Show issues Location:
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  7. Article ; Online: Multiple Transforming Growth Factor-β Isoforms and Receptors Function during Epithelial-Mesenchymal Cell Transformation in the Embryonic Heart

    Mercado-Pimentel, Melania E. / Runyan, Raymond B.

    Cells Tissues Organs - in vivo, in vitro

    2007  Volume 185, Issue 1-3, Page(s) 146–156

    Abstract: Epithelial-mesenchymal cell transformation (EMT) is a critical process during development of the heart valves. Transition of endothelial cells into mesenchymal cells in the atrioventricular (AV) canal and the outflow tract regions of the heart form the ... ...

    Abstract Epithelial-mesenchymal cell transformation (EMT) is a critical process during development of the heart valves. Transition of endothelial cells into mesenchymal cells in the atrioventricular (AV) canal and the outflow tract regions of the heart form the cardiac cushions that eventually form the heart valves. Collagen gel invasion assay has aided in the identification of molecules that regulate EMT. Among those, transforming growth factor-β (TGF-β) ligands and receptors demonstrate a critical role during EMT. In the chick, TGF-β ligands and some receptors have specific functions during EMT. TGF-β2 mediates endothelial cell-cell activation and separation, and TGF-β3 mediates cell invasion into the extracellular matrix. Receptors involved in the EMT process include TGF-β receptor type II (TBRII), TBRIII, endoglin and the TBRI receptors, ALK2 and ALK5. In contrast, in the mouse model, TGF-β2 is the only ligand involved in EMT. The TGF-β2 null mouse has either increased EMT or a mesenchymal cell proliferation after EMT. However, functional studies of TGF-β1 in vivo and in vitro showed that TGF-β1 functions in the EMT of the mouse AV canal. Latent TGF-β-binding protein (LTBP-1) and endoglin have a role in the EMT process. Therefore, TGF-βs mediate cardiac EMT in both embryonic species. Further studies will reveal the identification of ligand and receptor-specific activities.
    Keywords Endoglin ; ALK5 ; ALK2 ; Transforming growth factor-β2 ; Transforming growth factor-β3
    Language English
    Publisher S. Karger AG
    Publishing place Basel
    Publishing country Switzerland
    Document type Article ; Online
    ZDB-ID 1468141-9
    ISSN 1422-6421 ; 1422-6405 ; 1422-6405
    ISSN (online) 1422-6421
    ISSN 1422-6405
    DOI 10.1159/000101315
    Database Karger publisher's database

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  8. Article: Multiple Transforming Growth Factor-β Isoforms and Receptors Function during Epithelial-Mesenchymal Cell Transformation in the Embryonic Heart

    Mercado-Pimentel, Melania E. / Runyan, Raymond B.

    Cells Tissues Organs

    2007  Volume 185, Issue 1-3, Page(s) 146–156

    Abstract: Epithelial-mesenchymal cell transformation (EMT) is a critical process during development of the heart valves. Transition of endothelial cells into mesenchymal cells in the atrioventricular (AV) canal and the outflow tract regions of the heart form the ... ...

    Institution Departments of Cell Biology and Anatomy, University of Arizona, Tucson, Ariz., USA
    Abstract Epithelial-mesenchymal cell transformation (EMT) is a critical process during development of the heart valves. Transition of endothelial cells into mesenchymal cells in the atrioventricular (AV) canal and the outflow tract regions of the heart form the cardiac cushions that eventually form the heart valves. Collagen gel invasion assay has aided in the identification of molecules that regulate EMT. Among those, transforming growth factor-β (TGF-β) ligands and receptors demonstrate a critical role during EMT. In the chick, TGF-β ligands and some receptors have specific functions during EMT. TGF-β2 mediates endothelial cell-cell activation and separation, and TGF-β3 mediates cell invasion into the extracellular matrix. Receptors involved in the EMT process include TGF-β receptor type II (TBRII), TBRIII, endoglin and the TBRI receptors, ALK2 and ALK5. In contrast, in the mouse model, TGF-β2 is the only ligand involved in EMT. The TGF-β2 null mouse has either increased EMT or a mesenchymal cell proliferation after EMT. However, functional studies of TGF-β1 in vivo and in vitro showed that TGF-β1 functions in the EMT of the mouse AV canal. Latent TGF-β-binding protein (LTBP-1) and endoglin have a role in the EMT process. Therefore, TGF-βs mediate cardiac EMT in both embryonic species. Further studies will reveal the identification of ligand and receptor-specific activities.
    Keywords Transforming growth factor-β3 ; Endoglin ; ALK5 ; ALK2 ; Transforming growth factor-β2
    Language English
    Publishing date 2007-06-25
    Publisher S. Karger AG
    Publishing place Basel, Switzerland
    Document type Article
    Note Paper
    ZDB-ID 1468141-9
    ISBN 978-3-8055-8252-0 ; 978-3-318-01445-7 ; 3-8055-8252-8 ; 3-318-01445-1
    ISSN 1422-6421 ; 1422-6405
    ISSN (online) 1422-6421
    ISSN 1422-6405
    DOI 10.1159/000101315
    Database Karger publisher's database

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  9. Article: S100P/RAGE signaling regulates microRNA-155 expression via AP-1 activation in colon cancer

    Onyeagucha, Benjamin Chidi / Mercado-Pimentel, Melania E / Hutchison, Jennifer / Flemington, Erik K / Nelson, Mark A

    Experimental cell research. 2013 Aug. 1, v. 319, no. 13

    2013  

    Abstract: Accumulating evidence indicates that elevated S100P promotes the pathogenesis of cancers, including colon cancer. S100P exerts its effects by binding to and activating the Receptor for Advance Glycation End-products (RAGE). The effects of up-regulated ... ...

    Abstract Accumulating evidence indicates that elevated S100P promotes the pathogenesis of cancers, including colon cancer. S100P exerts its effects by binding to and activating the Receptor for Advance Glycation End-products (RAGE). The effects of up-regulated S100P/RAGE signaling on cell functions are well documented. Despite these observations, little is known about the downstream targets of S100P/RAGE signaling. In the present study, we demonstrated for the first time that activation of RAGE by S100P regulates oncogenic microRNA-155 (miR-155) expression through Activator Protein-1 (AP-1) stimulation in colon cancer cells. Ectopic S100P up-regulated miR-155 levels in human colon cancer cells. Conversely, knockdown of S100P resulted in a decrease in miR-155 levels. Exogenous S100P induced miR-155 expression, but blockage of the RAGE with anti-RAGE antibody suppressed the induction of miR-155 by exogenous S100P. Attenuation of AP-1 activation through pharmacological inhibition of MEK activation or genetic inhibition of c-Jun activation using dominant negative c-Jun (TAM67) suppressed miR-155 induction by exogenous S100P. Also, S100P treatment stimulated the enrichment of c-Fos, an AP-1 family member, at the miR-155 host gene promoter site. Finally, a functional study demonstrated that miR-155 knockdown decreases colon cancer cell growth, motility, and invasion. Altogether, these data demonstrate that the expression of miR-155 is regulated by S100P and is dependent on RAGE activation and stimulation of AP-1.
    Keywords antibodies ; cell growth ; colorectal neoplasms ; genes ; glycation ; humans ; neoplasm cells ; pathogenesis
    Language English
    Dates of publication 2013-0801
    Size p. 2081-2090.
    Publishing place Elsevier Inc.
    Document type Article
    ZDB-ID 1493-x
    ISSN 1090-2422 ; 0014-4827
    ISSN (online) 1090-2422
    ISSN 0014-4827
    DOI 10.1016/j.yexcr.2013.05.009
    Database NAL-Catalogue (AGRICOLA)

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  10. Article: TGF beta-mediated RhoA expression is necessary for epithelial-mesenchymal transition in the embryonic chick heart.

    Tavares, André Luiz P / Mercado-Pimentel, Melania E / Runyan, Raymond B / Kitten, Gregory T

    Developmental dynamics : an official publication of the American Association of Anatomists

    2006  Volume 235, Issue 6, Page(s) 1589–1598

    Abstract: Endothelia in the atrioventricular canal (AVC) of the embryonic heart undergo an epithelial-mesenchymal transition (EMT) and migrate into the underlying extracellular matrix. We explore here whether RhoA mediates this EMT. RhoA was detected in all cells ... ...

    Abstract Endothelia in the atrioventricular canal (AVC) of the embryonic heart undergo an epithelial-mesenchymal transition (EMT) and migrate into the underlying extracellular matrix. We explore here whether RhoA mediates this EMT. RhoA was detected in all cells of the chick heart during the stages studied. Expression was elevated when EMT was actively occurring. Explants treated with C3 exoenzyme in collagen gel cultures showed a significant decrease in mesenchymal cell numbers. siRNA was used to inhibit RhoA mRNA, and both activated endothelial and mesenchymal cells decreased significantly with treatment. Loss of RhoA produced a reduction of RhoB, cyclin-b2, and beta-catenin messages showing that these genes are regulated downstream of RhoA. In contrast, runx-2 was not reduced. Inhibition of TGFbeta3 or TGFbeta2 activity caused a large reduction of RhoA message. These data place RhoA in TGFbeta regulated pathways for both endothelial activation and mesenchymal invasion and demonstrate a functional requirement during EMT.
    MeSH term(s) Animals ; Chick Embryo ; Epithelium/embryology ; Heart/embryology ; Mesoderm/physiology ; Transforming Growth Factor beta/physiology ; rhoA GTP-Binding Protein/biosynthesis ; rhoA GTP-Binding Protein/genetics
    Chemical Substances Transforming Growth Factor beta ; rhoA GTP-Binding Protein (EC 3.6.5.2)
    Language English
    Publishing date 2006-06
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 1102541-4
    ISSN 1097-0177 ; 1058-8388
    ISSN (online) 1097-0177
    ISSN 1058-8388
    DOI 10.1002/dvdy.20771
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