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  1. Article ; Online: The role of the miR-200 family in epithelial-mesenchymal transition.

    Mongroo, Perry S / Rustgi, Anil K

    Cancer biology & therapy

    2010  Volume 10, Issue 3, Page(s) 219–222

    Abstract: MicroRNAs (miRNAs) are single-stranded, non-coding RNA molecules that regulate gene expression at the post-transcriptional level. Genes encoding miRNAs are located in regions of the genome that are commonly amplified, deleted or rearranged. They are ... ...

    Abstract MicroRNAs (miRNAs) are single-stranded, non-coding RNA molecules that regulate gene expression at the post-transcriptional level. Genes encoding miRNAs are located in regions of the genome that are commonly amplified, deleted or rearranged. They are commonly dysregulated in human cancers and known to act as oncogenes or tumor suppressors. Members of the miR-200 miRNA family are downregulated in human cancer cells and tumors due to aberrant epigenetic gene silencing and play a critical role in the suppression of epithelial-to-mesenchymal transition (EMT), tumor cell adhesion, migration, invasion and metastasis, by targeting and repressing the expression of key mRNAs that are involved in EMT (ZEB1 and ZEB2), β-catenin/Wnt signaling (β-catenin), EGFR inhibitor resistance (ERRFI-1) and chemoresistance to therapeutic agents (TUBB3). Since the miR-200 family functions as putative tumor suppressors and represent biomarkers for poorly differentiated and aggressive cancers, restoration of miR-200 expression may have therapeutic implications for the treatment of metastatic and drug-resistant tumors.
    MeSH term(s) Epithelial Cells/cytology ; Epithelial Cells/metabolism ; Epithelial-Mesenchymal Transition/genetics ; Gene Expression Regulation, Neoplastic ; Humans ; MicroRNAs/genetics ; MicroRNAs/metabolism ; MicroRNAs/physiology ; Neoplasms/genetics ; Neoplasms/metabolism ; Neoplasms/pathology ; beta Catenin/genetics ; beta Catenin/metabolism
    Chemical Substances MicroRNAs ; beta Catenin
    Language English
    Publishing date 2010-08-01
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2146305-0
    ISSN 1555-8576 ; 1538-4047
    ISSN (online) 1555-8576
    ISSN 1538-4047
    DOI 10.4161/cbt.10.3.12548
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Does MicroRNA microarray for the microsatellite status have a big translational impact?

    Mongroo, Perry S / King, Catrina / Nakagawa, Hiroshi

    Gastroenterology

    2009  Volume 136, Issue 3, Page(s) 1112–4; discussion 1114

    Language English
    Publishing date 2009-03
    Publishing country United States
    Document type Comment ; Journal Article
    ZDB-ID 80112-4
    ISSN 1528-0012 ; 0016-5085
    ISSN (online) 1528-0012
    ISSN 0016-5085
    DOI 10.1053/j.gastro.2009.01.031
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  3. Article ; Online: IMP-1 displays cross-talk with K-Ras and modulates colon cancer cell survival through the novel proapoptotic protein CYFIP2.

    Mongroo, Perry S / Noubissi, Felicite K / Cuatrecasas, Miriam / Kalabis, Jiri / King, Catrina E / Johnstone, Cameron N / Bowser, Mark J / Castells, Antoni / Spiegelman, Vladimir S / Rustgi, Anil K

    Cancer research

    2011  Volume 71, Issue 6, Page(s) 2172–2182

    Abstract: Insulin-like growth factor 2 mRNA-binding protein-1 (IMP-1) is an oncofetal protein that binds directly to and stabilizes oncogenic c-Myc and regulates, in turn, its posttranscriptional expression and translation. In contrast to normal adult tissue, IMP- ... ...

    Abstract Insulin-like growth factor 2 mRNA-binding protein-1 (IMP-1) is an oncofetal protein that binds directly to and stabilizes oncogenic c-Myc and regulates, in turn, its posttranscriptional expression and translation. In contrast to normal adult tissue, IMP-1 is reexpressed and/or overexpressed in human cancers. We show that knockdown of c-Myc in human colon cancer cell lines increases the expression of mature let-7 miRNA family members and downregulates several of its mRNA targets: IMP-1, Cdc34, and K-Ras. We further show that loss of IMP-1 inhibits Cdc34, Lin-28B, and K-Ras, suppresses SW-480 cell proliferation and anchorage-independent growth, and promotes caspase- and lamin-mediated cell death. We also found that IMP-1 binds to the coding region and 3'UTR of K-Ras mRNA. RNA microarray profiling and validation by reverse transcription PCR reveals that the p53-inducible proapoptotic protein CYFIP2 is upregulated in IMP-1 knockdown SW480 cells, a novel finding. We also show that overexpression of IMP-1 increases c-Myc and K-Ras expression and LIM2405 cell proliferation. Furthermore, we show that loss of IMP-1 induces Caspase-3- and PARP-mediated apoptosis, and inhibits K-Ras expression in SW480 cells, which is rescued by CYFIP2 knockdown. Importantly, analysis of 228 patients with colon cancers reveals that IMP-1 is significantly upregulated in differentiated colon tumors (P ≤ 0.0001) and correlates with K-Ras expression (r = 0.35, P ≤ 0.0001) relative to adjacent normal mucosa. These findings indicate that IMP-1, interrelated with c-Myc, acts upstream of K-Ras to promote survival through a novel mechanism that may be important in colon cancer pathogenesis.
    MeSH term(s) 3' Untranslated Regions/genetics ; Adaptor Proteins, Signal Transducing/genetics ; Adaptor Proteins, Signal Transducing/metabolism ; Apoptosis ; Caco-2 Cells ; Cell Line, Tumor ; Cell Proliferation ; Cell Survival ; Colonic Neoplasms/genetics ; Colonic Neoplasms/metabolism ; Colonic Neoplasms/pathology ; Female ; Humans ; Immunoblotting ; Male ; Protein Binding ; Proto-Oncogene Proteins c-myc/genetics ; Proto-Oncogene Proteins c-myc/metabolism ; RNA Interference ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; RNA-Binding Proteins/genetics ; RNA-Binding Proteins/metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; Tissue Array Analysis ; Up-Regulation ; ras Proteins/genetics ; ras Proteins/metabolism
    Chemical Substances 3' Untranslated Regions ; Adaptor Proteins, Signal Transducing ; CYFIP2 protein, human ; IGF2BP1 protein, human ; MYC protein, human ; Proto-Oncogene Proteins c-myc ; RNA, Messenger ; RNA-Binding Proteins ; ras Proteins (EC 3.6.5.2)
    Language English
    Publishing date 2011-01-20
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 1432-1
    ISSN 1538-7445 ; 0008-5472
    ISSN (online) 1538-7445
    ISSN 0008-5472
    DOI 10.1158/0008-5472.CAN-10-3295
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article: Beta-parvin inhibits integrin-linked kinase signaling and is downregulated in breast cancer.

    Mongroo, Perry S / Johnstone, Cameron N / Naruszewicz, Izabela / Leung-Hagesteijn, Chungyee / Sung, Raphael K / Carnio, Leanne / Rustgi, Anil K / Hannigan, Gregory E

    Oncogene

    2004  Volume 23, Issue 55, Page(s) 8959–8970

    Abstract: We analysed breast tumors and breast cancer cell lines for the expression of beta-parvin (ParvB), an adaptor protein that binds to the integrin-linked kinase (ILK). Quantitative RT-PCR indicated that ParvB mRNA was downregulated, by at least 60%, in four ...

    Abstract We analysed breast tumors and breast cancer cell lines for the expression of beta-parvin (ParvB), an adaptor protein that binds to the integrin-linked kinase (ILK). Quantitative RT-PCR indicated that ParvB mRNA was downregulated, by at least 60%, in four of nine breast tumors, relative to patient-matched normal mammary gland tissue. We also found that ParvB protein levels were reduced by > or =90% in five of seven advanced tumors, relative to matched normal breast tissue. Conversely, ILK protein and kinase activity levels were elevated in these tumors, suggesting that downregulation of ParvB stimulates ILK signaling. Western blot analyses indicated very low levels of ParvB protein in MDA-MB-231 and MCF7 breast cancer cells, facilitating functional studies of the effects of ParvB on ILK signaling. Expression of ParvB in MDA-MB-231 and MCF7 cells increased cell adhesion to collagen. ParvB inhibited ILK kinase activity, anchorage-independent cell growth and in vitro matrigel invasion by MDA-MB-231 cells. EGF-induced phosphorylation of two ILK targets, PKB (Ser473) and glycogen synthase kinase 3beta (Ser9), was also inhibited by ParvB. These results indicated that ParvB inhibits ILK signaling downstream of receptor tyrosine kinases. Our results suggest that loss of ParvB expression is a novel mechanism for upregulating ILK activity in tumors.
    MeSH term(s) Actinin/metabolism ; Adenoviridae/genetics ; Amino Acid Sequence ; Antibodies/chemistry ; Blotting, Western ; Breast Neoplasms/metabolism ; Breast Neoplasms/pathology ; Cell Adhesion ; Cell Cycle ; Cell Line, Tumor ; Cell Proliferation ; Collagen/chemistry ; Collagen/metabolism ; Collagen/pharmacology ; Coloring Agents/pharmacology ; DNA, Complementary/metabolism ; Down-Regulation ; Drug Combinations ; Epidermal Growth Factor/metabolism ; Genes, Reporter ; Glycogen Synthase Kinase 3/metabolism ; Glycogen Synthase Kinase 3 beta ; Humans ; Laminin/chemistry ; Laminin/pharmacology ; Models, Genetic ; Molecular Sequence Data ; Phosphorylation ; Plasmids/metabolism ; Protein Structure, Tertiary ; Protein-Serine-Threonine Kinases/metabolism ; Proteoglycans/chemistry ; Proteoglycans/pharmacology ; RNA, Messenger/metabolism ; Recombinant Proteins/chemistry ; Reverse Transcriptase Polymerase Chain Reaction ; Signal Transduction ; Tetrazolium Salts/pharmacology ; Thiazoles/pharmacology ; Transfection ; Two-Hybrid System Techniques ; Up-Regulation
    Chemical Substances Antibodies ; Coloring Agents ; DNA, Complementary ; Drug Combinations ; Laminin ; PARVB protein, human ; Proteoglycans ; RNA, Messenger ; Recombinant Proteins ; Tetrazolium Salts ; Thiazoles ; Actinin (11003-00-2) ; matrigel (119978-18-6) ; Epidermal Growth Factor (62229-50-9) ; Collagen (9007-34-5) ; integrin-linked kinase (EC 2.7.1.-) ; GSK3B protein, human (EC 2.7.11.1) ; Glycogen Synthase Kinase 3 beta (EC 2.7.11.1) ; Protein-Serine-Threonine Kinases (EC 2.7.11.1) ; Glycogen Synthase Kinase 3 (EC 2.7.11.26) ; thiazolyl blue (EUY85H477I)
    Language English
    Publishing date 2004-11-25
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, U.S. Gov't, P.H.S.
    ZDB-ID 639046-8
    ISSN 1476-5594 ; 0950-9232
    ISSN (online) 1476-5594
    ISSN 0950-9232
    DOI 10.1038/sj.onc.1208112
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Parvin-beta inhibits breast cancer tumorigenicity and promotes CDK9-mediated peroxisome proliferator-activated receptor gamma 1 phosphorylation.

    Johnstone, Cameron N / Mongroo, Perry S / Rich, A Sophie / Schupp, Michael / Bowser, Mark J / Delemos, Andrew S / Tobias, John W / Liu, Yingqiu / Hannigan, Gregory E / Rustgi, Anil K

    Molecular and cellular biology

    2007  Volume 28, Issue 2, Page(s) 687–704

    Abstract: Parvin-beta is a focal adhesion protein downregulated in human breast cancer cells. Loss of Parvin-beta contributes to increased integrin-linked kinase activity, cell-matrix adhesion, and invasion through the extracellular matrix in vitro. The effect of ... ...

    Abstract Parvin-beta is a focal adhesion protein downregulated in human breast cancer cells. Loss of Parvin-beta contributes to increased integrin-linked kinase activity, cell-matrix adhesion, and invasion through the extracellular matrix in vitro. The effect of ectopic Parvin-beta expression on the transcriptional profile of MDA-MB-231 breast cancer cells, which normally do not express Parvin-beta, was evaluated. Particular emphasis was placed upon propagating MDA-MB-231 breast cancer cells in three-dimensional culture matrices. Interestingly, Parvin-beta reexpression in MDA-MB-231 cells increased the mRNA expression, serine 82 phosphorylation (mediated by CDK9), and activity of the nuclear hormone receptor peroxisome proliferator-activated receptor gamma (PPARgamma), and there was a concomitant increase in lipogenic gene expression as a downstream effector of PPARgamma. Importantly, Parvin-beta suppressed breast cancer growth in vivo, with associated decreased proliferation. These data suggest that Parvin-beta might influence breast cancer progression.
    MeSH term(s) Actinin/genetics ; Actinin/metabolism ; Animals ; Breast Neoplasms/genetics ; Breast Neoplasms/metabolism ; Breast Neoplasms/pathology ; Cell Differentiation ; Cell Line, Tumor ; Cell Proliferation ; Cell Transformation, Neoplastic/genetics ; Cell Transformation, Neoplastic/metabolism ; Cell Transformation, Neoplastic/pathology ; Cyclin-Dependent Kinase 9/genetics ; Cyclin-Dependent Kinase 9/metabolism ; Gene Expression Profiling ; Gene Expression Regulation, Neoplastic ; Humans ; Lipid Metabolism ; Mice ; Neoplasm Transplantation ; PPAR gamma/genetics ; PPAR gamma/metabolism ; Phosphorylation ; Phosphoserine/metabolism ; RNA, Messenger/genetics ; Transcription, Genetic/genetics
    Chemical Substances PARVB protein, human ; PPAR gamma ; RNA, Messenger ; Actinin (11003-00-2) ; Phosphoserine (17885-08-4) ; Cyclin-Dependent Kinase 9 (EC 2.7.11.22)
    Language English
    Publishing date 2007-11-12
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 779397-2
    ISSN 1098-5549 ; 0270-7306
    ISSN (online) 1098-5549
    ISSN 0270-7306
    DOI 10.1128/MCB.01617-06
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Integrin-linked kinase expression is elevated in human cardiac hypertrophy and induces hypertrophy in transgenic mice.

    Lu, Huanzhang / Fedak, Paul W M / Dai, Xiaojing / Du, Changqing / Zhou, Yu-Qing / Henkelman, Mark / Mongroo, Perry S / Lau, Arthur / Yamabi, Hideaki / Hinek, Aleksander / Husain, Mansoor / Hannigan, Gregory / Coles, John G

    Circulation

    2006  Volume 114, Issue 21, Page(s) 2271–2279

    Abstract: Background: Although numerous signaling pathways are known to be activated in experimental cardiac hypertrophy, the molecular basis of the hypertrophic response inherent in human heart diseases remains largely unknown. Integrin-linked kinase (ILK) is a ... ...

    Abstract Background: Although numerous signaling pathways are known to be activated in experimental cardiac hypertrophy, the molecular basis of the hypertrophic response inherent in human heart diseases remains largely unknown. Integrin-linked kinase (ILK) is a multifunctional protein kinase that physically links beta-integrins with the actin cytoskeleton, suggesting a potential mechanoreceptor role.
    Methods and results: Here, we show a marked increase in ILK protein levels in hypertrophic ventricles of patients with congenital and acquired outflow tract obstruction. This increase in ILK was associated with activation of the Rho family guanine triphosphatases, Rac1 and Cdc42, and known hypertrophic signaling kinases, including extracellular signal-related kinases (ERK1/2) and p70 S6 kinase. Transgenic mice with cardiac-specific expression of a constitutively active ILK (ILK(S343D)) or wild-type ILK (ILK(WT)) exhibited a compensated ventricular hypertrophic phenotype and displayed an activation profile of guanine triphosphatases and downstream protein kinases concordant with that seen in human hypertrophy. In contrast, transgenic mice with cardiomyocyte-restricted expression of a kinase-inactive ILK (ILK(R211A)) were unable to mount a compensatory hypertrophic response to angiotensin II in vivo.
    Conclusions: Taken together, these results identify ILK-regulated signaling as a broadly adaptive hypertrophic response mechanism relevant to a wide range of clinical heart disease.
    MeSH term(s) Alanine ; Angiotensin II ; Animals ; Arginine ; Cardiomegaly/enzymology ; Cardiomegaly/etiology ; Enzyme Activation ; Extracellular Signal-Regulated MAP Kinases/metabolism ; Fetus/enzymology ; Heart Ventricles ; Humans ; Infant ; Mice ; Mice, Transgenic ; Mutation ; Myocardium/enzymology ; Myocytes, Cardiac/metabolism ; Phosphorylation ; Protein-Serine-Threonine Kinases/genetics ; Protein-Serine-Threonine Kinases/metabolism ; Ribosomal Protein S6 Kinases, 70-kDa/metabolism ; Ventricular Outflow Obstruction/congenital ; Ventricular Outflow Obstruction/enzymology ; cdc42 GTP-Binding Protein/metabolism ; rac1 GTP-Binding Protein/metabolism
    Chemical Substances Angiotensin II (11128-99-7) ; Arginine (94ZLA3W45F) ; integrin-linked kinase (EC 2.7.1.-) ; Protein-Serine-Threonine Kinases (EC 2.7.11.1) ; Ribosomal Protein S6 Kinases, 70-kDa (EC 2.7.11.1) ; Extracellular Signal-Regulated MAP Kinases (EC 2.7.11.24) ; cdc42 GTP-Binding Protein (EC 3.6.5.2) ; rac1 GTP-Binding Protein (EC 3.6.5.2) ; Alanine (OF5P57N2ZX)
    Language English
    Publishing date 2006-11-21
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 80099-5
    ISSN 1524-4539 ; 0009-7322 ; 0069-4193 ; 0065-8499
    ISSN (online) 1524-4539
    ISSN 0009-7322 ; 0069-4193 ; 0065-8499
    DOI 10.1161/CIRCULATIONAHA.106.642330
    Database MEDical Literature Analysis and Retrieval System OnLINE

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