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  1. Article ; Online: Rab25 in cancer: a brief update.

    Mitra, Shreya / Cheng, Kwai W / Mills, Gordon B

    Biochemical Society transactions

    2012  Volume 40, Issue 6, Page(s) 1404–1408

    Abstract: Derailed endocytosis is a hallmark of cancer. The endocytic pathway, as demonstrated by our laboratory, is a frequent target of genomic aberrations in cancer and plays a critical role in the maintenance of cellular polarity, stem cell function, ... ...

    Abstract Derailed endocytosis is a hallmark of cancer. The endocytic pathway, as demonstrated by our laboratory, is a frequent target of genomic aberrations in cancer and plays a critical role in the maintenance of cellular polarity, stem cell function, bioenergetics, proliferation, motility, invasion, metastasis, apoptosis and autophagy. The Rab GTPases, along with their effectors, are critical regulators of this endocytic machinery and can have a huge impact on the cellular itinerary of growth and metabolism. Rab25 is an epithelial-cell-specific member of the Rab GTPase superfamily, sharing close homology with Rab11a, the endosomal recycling Rab GTPase. RAB25 has been implicated in various cancers, with reports presenting it as both an oncogene and a tumour-suppressor gene. At the cellular level, Rab25 was shown to contribute to invasiveness of cancer cells by regulating integrin trafficking. Recently, our laboratory uncovered a critical role for Rab25 in cellular energetics. Assimilating all of the existing evidence, in the present review, we give an updated overview of the complex and often context-dependent role of Rab25 in cancer.
    MeSH term(s) Animals ; Disease Progression ; Genes, Tumor Suppressor ; Humans ; Neoplasms/enzymology ; Neoplasms/genetics ; Neoplasms/pathology ; Oncogenes ; Protein Transport ; rab GTP-Binding Proteins/genetics ; rab GTP-Binding Proteins/metabolism ; rab GTP-Binding Proteins/physiology
    Chemical Substances Rab25 protein, human ; rab GTP-Binding Proteins (EC 3.6.5.2)
    Language English
    Publishing date 2012-11-24
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 184237-7
    ISSN 1470-8752 ; 0300-5127
    ISSN (online) 1470-8752
    ISSN 0300-5127
    DOI 10.1042/BST20120249
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 944: Show issues Location:
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  2. Article: Rab GTPases implicated in inherited and acquired disorders

    Mitra, Shreya / Cheng, Kwai W / Mills, Gordon B

    Seminars in cell & developmental biology. 2011 Feb., v. 22, no. 1

    2011  

    Abstract: The endocytotic machinery imports, transports and exports receptors and associated molecules between the plasma membrane and various cytoplasmic chambers resulting in selective recycling, degradation, or secretion of molecules and signaling complexes. ... ...

    Abstract The endocytotic machinery imports, transports and exports receptors and associated molecules between the plasma membrane and various cytoplasmic chambers resulting in selective recycling, degradation, or secretion of molecules and signaling complexes. Trafficking of receptors, growth factors, nutrients, cytokines, integrins as well as pathogens dictates the kinetics and magnitude of signal transduction cascades. Understandably, alterations in the ‘fate’ of such cargo complexes have profound physiologic and pathophysiologic implications. Rab GTPases regulate endocytosis by decorating intracellular vesicles and targeting these vesicles along with their cargoes to appropriate subcellular compartments. In the last decade, the number of genetic diseases driven by germline mutations in Rab GTPases or their interacting proteins [1–3], has increased and there is growing evidence of aberrant Rab GTPase function in acquired pathophysiologies such as immune deficiency, infection, obesity, diabetes and cancer.
    Keywords guanosinetriphosphatase ; germ cells ; secretion ; immunosuppression ; nutrients ; cytokines ; mutation ; endocytosis ; genetic disorders ; receptors ; signal transduction ; obesity ; plasma membrane ; diabetes ; integrins ; growth factors ; pathogens
    Language English
    Dates of publication 2011-02
    Size p. 57-68.
    Publishing place Elsevier Ltd
    Document type Article
    Note 2019-12-04
    ZDB-ID 1312473-0
    ISSN 1096-3634 ; 1084-9521
    ISSN (online) 1096-3634
    ISSN 1084-9521
    DOI 10.1016/j.semcdb.2010.12.005
    Database NAL-Catalogue (AGRICOLA)

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  3. Article ; Online: Rab GTPases implicated in inherited and acquired disorders.

    Mitra, Shreya / Cheng, Kwai W / Mills, Gordon B

    Seminars in cell & developmental biology

    2010  Volume 22, Issue 1, Page(s) 57–68

    Abstract: The endocytotic machinery imports, transports and exports receptors and associated molecules between the plasma membrane and various cytoplasmic chambers resulting in selective recycling, degradation, or secretion of molecules and signaling complexes. ... ...

    Abstract The endocytotic machinery imports, transports and exports receptors and associated molecules between the plasma membrane and various cytoplasmic chambers resulting in selective recycling, degradation, or secretion of molecules and signaling complexes. Trafficking of receptors, growth factors, nutrients, cytokines, integrins as well as pathogens dictates the kinetics and magnitude of signal transduction cascades. Understandably, alterations in the 'fate' of such cargo complexes have profound physiologic and pathophysiologic implications. Rab GTPases regulate endocytosis by decorating intracellular vesicles and targeting these vesicles along with their cargoes to appropriate subcellular compartments. In the last decade, the number of genetic diseases driven by germline mutations in Rab GTPases or their interacting proteins, has increased and there is growing evidence of aberrant Rab GTPase function in acquired pathophysiologies such as immune deficiency, infection, obesity, diabetes and cancer.
    MeSH term(s) Animals ; Biological Transport ; Endocytosis ; Genetic Predisposition to Disease ; Humans ; Mutation ; Transport Vesicles/enzymology ; rab GTP-Binding Proteins/genetics ; rab GTP-Binding Proteins/metabolism
    Chemical Substances rab GTP-Binding Proteins (EC 3.6.5.2)
    Language English
    Publishing date 2010-12-13
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 1312473-0
    ISSN 1096-3634 ; 1084-9521
    ISSN (online) 1096-3634
    ISSN 1084-9521
    DOI 10.1016/j.semcdb.2010.12.005
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Rab25 acts as an oncogene in luminal B breast cancer and is causally associated with Snail driven EMT.

    Mitra, Shreya / Federico, Lorenzo / Zhao, Wei / Dennison, Jennifer / Sarkar, Tapasree Roy / Zhang, Fan / Takiar, Vinita / Cheng, Kwai W / Mani, Sendurai / Lee, Ju Seog / Mills, Gordon B

    Oncotarget

    2016  Volume 7, Issue 26, Page(s) 40252–40265

    Abstract: The Rab GTPases regulate vesicular trafficking machinery that transports and delivers a diverse pool of cargo, including growth factor receptors, integrins, nutrient receptors and junction proteins to specific intracellular sites. The trafficking ... ...

    Abstract The Rab GTPases regulate vesicular trafficking machinery that transports and delivers a diverse pool of cargo, including growth factor receptors, integrins, nutrient receptors and junction proteins to specific intracellular sites. The trafficking machinery is indeed a major posttranslational modifier and is critical for cellular homeostasis. Deregulation of this stringently controlled system leads to a wide spectrum of disorders including cancer. Herein we demonstrate that Rab25, a key GTPase, mostly decorating the apical recycling endosome, is a dichotomous variable in breast cancer cell lines with higher mRNA and protein expression in Estrogen Receptor positive (ER+ve) lines. Rab25 and its effector, Rab Coupling Protein (RCP) are frequently coamplified and coordinately elevated in ER+ve breast cancers. In contrast, Rab25 levels are decreased in basal-like and almost completely lost in claudin-low tumors. This dichotomy exists despite the presence of the 1q amplicon that hosts Rab25 across breast cancer subtypes and is likely due to differential methylation of the Rab25 promoter. Functionally, elevated levels of Rab25 drive major hallmarks of cancer including indefinite growth and metastasis but in case of luminal B breast cancer only. Importantly, in such ER+ve tumors, coexpression of Rab25 and its effector, RCP is significantly associated with a markedly worsened clinical outcome. Importantly, in claudin-low cell lines, exogenous Rab25 markedly inhibits cell migration. Similarly, during Snail-induced epithelial to mesenchymal transition (EMT) exogenous Rab25 potently reverses Snail-driven invasion. Overall, this study substantiates a striking context dependent role of Rab25 in breast cancer where Rab25 is amplified and enhances aggressiveness in luminal B cancers while in claudin-low tumors, Rab25 is lost indicating possible anti-tumor functions.
    Language English
    Publishing date 2016-06-28
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2560162-3
    ISSN 1949-2553 ; 1949-2553
    ISSN (online) 1949-2553
    ISSN 1949-2553
    DOI 10.18632/oncotarget.9730
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article: Emerging role of RAB GTPases in cancer and human disease.

    Cheng, Kwai W / Lahad, John P / Gray, Joseph W / Mills, Gordon B

    Cancer research

    2005  Volume 65, Issue 7, Page(s) 2516–2519

    Abstract: Emerging evidence implicates alterations in the RAB small GTPases and their associated regulatory proteins and effectors in multiple human diseases including cancer. We have recently shown that RAB25, located at chromosome 1q22, is amplified at the DNA ... ...

    Abstract Emerging evidence implicates alterations in the RAB small GTPases and their associated regulatory proteins and effectors in multiple human diseases including cancer. We have recently shown that RAB25, located at chromosome 1q22, is amplified at the DNA level and overexpressed at the RNA level in ovarian and breast cancer. These changes correlated with a worsened outcome in both diseases. In addition, enforced expression of RAB25 in both breast and ovarian cancer cells decreased apoptosis and increased proliferation and aggressiveness in vivo, potentially explaining the worsened prognosis. A better understanding of genetic alterations as well as the physiologic and pathophysiologic roles of RAB GTPases may open new opportunities for therapeutic intervention and better outcomes.
    MeSH term(s) Breast Neoplasms/enzymology ; Breast Neoplasms/pathology ; Female ; Humans ; Ovarian Neoplasms/enzymology ; Ovarian Neoplasms/pathology ; rab GTP-Binding Proteins/physiology
    Chemical Substances rab GTP-Binding Proteins (EC 3.6.5.2)
    Language English
    Publishing date 2005-04-01
    Publishing country United States
    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. ; Review
    ZDB-ID 1432-1
    ISSN 1538-7445 ; 0008-5472
    ISSN (online) 1538-7445
    ISSN 0008-5472
    DOI 10.1158/0008-5472.CAN-05-0573
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article: Role of decreased levels of lipid phosphate phosphatase-1 in accumulation of lysophosphatidic acid in ovarian cancer.

    Tanyi, Janos L / Hasegawa, Yutaka / Lapushin, Ruth / Morris, Andrew J / Wolf, Judith K / Berchuck, Andrew / Lu, Karen / Smith, David I / Kalli, Kimberly / Hartmann, Lynn C / McCune, Karen / Fishman, David / Broaddus, Russell / Cheng, Kwai W / Atkinson, Edward N / Yamal, Jose M / Bast, Robert C / Felix, Edward A / Newman, Robert A /
    Mills, Gordon B

    Clinical cancer research : an official journal of the American Association for Cancer Research

    2003  Volume 9, Issue 10 Pt 1, Page(s) 3534–3545

    Abstract: The levels of lysophosphatidic acid (LPA) are consistently elevated in the ascites of ovarian cancer patients, suggesting that ovarian cancer cells are exposed to an LPA replete environment. LPA stimulates cell proliferation, cell survival, resistance to ...

    Abstract The levels of lysophosphatidic acid (LPA) are consistently elevated in the ascites of ovarian cancer patients, suggesting that ovarian cancer cells are exposed to an LPA replete environment. LPA stimulates cell proliferation, cell survival, resistance to cisplatin, production and activation of proteases, invasiveness and production of the neovascularizing factors, vascular endothelial growth factor, and interleukin 8. Although ovarian cancer cells can produce LPA, this may not be the major reason for altered LPA levels in ascites. We have demonstrated that the major mechanism of degradation of LPA by ovarian cancer cells is through a lipid phosphate phosphatase (LPP)-like activity. We demonstrate herein that LPP-1 mRNA is decreased in the majority of ovarian cancers. This is recapitulated in ovarian cancer cell lines, where LPP-1 RNA levels are lower than those in normal ovarian epithelium and immortalized ovarian epithelial cells. Introduction of LPP-1 into ovarian cancer cell lines results in increased LPA hydrolysis, which is associated with a marked inhibition of cell proliferation and colony-forming activity and a marked increase in apoptosis. Thus, the LPA-rich environment of the ovarian cancer cell in vivo and the subsequent effects of cellular pathophysiology may be a consequence of both increased LPA production and decreased LPA metabolism by ovarian cancer cells.
    MeSH term(s) Cell Division ; Cell Line, Tumor ; Cell Movement ; Cell Survival ; DNA, Complementary/metabolism ; DNA-Binding Proteins ; Female ; Green Fluorescent Proteins ; Humans ; Hydrolysis ; Luminescent Proteins/metabolism ; Lysophospholipids/metabolism ; Oligonucleotide Array Sequence Analysis ; Ovarian Neoplasms/enzymology ; Ovarian Neoplasms/metabolism ; Phosphatidate Phosphatase/biosynthesis ; Phosphatidate Phosphatase/physiology ; Precipitin Tests ; Promoter Regions, Genetic ; RNA/metabolism ; RNA, Messenger/metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; Telomerase/metabolism ; Transfection
    Chemical Substances DNA, Complementary ; DNA-Binding Proteins ; Luminescent Proteins ; Lysophospholipids ; RNA, Messenger ; Green Fluorescent Proteins (147336-22-9) ; RNA (63231-63-0) ; Telomerase (EC 2.7.7.49) ; lipid phosphate phosphatase (EC 3.1.3.-) ; Phosphatidate Phosphatase (EC 3.1.3.4) ; lysophosphatidic acid (PG6M3969SG)
    Language English
    Publishing date 2003-09-01
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, P.H.S.
    ZDB-ID 1225457-5
    ISSN 1557-3265 ; 1078-0432
    ISSN (online) 1557-3265
    ISSN 1078-0432
    Database MEDical Literature Analysis and Retrieval System OnLINE

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