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  1. Article ; Online: Retraction: RNA interference-directed knockdown of urokinase plasminogen activator and urokinase plasminogen activator receptor inhibits prostate cancer cell invasion, survival, and tumorigenicity

    Pulukuri, Sai MuraliKrishna / Gondi, Christopher S / Lakka, Sajani S / Jutla, Aman / Estes, Norman / Gujrati, Meena / Rao, Jasti S

    The Journal of biological chemistry

    2020  Volume 295, Issue 37, Page(s) 13136

    Language English
    Publishing date 2020-09-11
    Publishing country United States
    Document type Journal Article ; Retraction of Publication
    ZDB-ID 2997-x
    ISSN 1083-351X ; 0021-9258
    ISSN (online) 1083-351X
    ISSN 0021-9258
    DOI 10.1074/jbc.RX120.015588
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article: RNA interference-directed knockdown of urokinase plasminogen activator and urokinase plasminogen activator receptor inhibits prostate cancer cell invasion, survival, and tumorigenicity in vivo.

    Pulukuri, Sai MuraliKrishna / Gondi, Christopher S / Lakka, Sajani S / Jutla, Aman / Estes, Norman / Gujrati, Meena / Rao, Jasti S

    publication RETRACTED

    The Journal of biological chemistry

    2005  Volume 280, Issue 43, Page(s) 36529–36540

    Abstract: The invasive ability of tumor cells plays a key role in prostate cancer metastasis and is a major cause of treatment failure. Urokinase plasminogen activator-(uPA) and its receptor (uPAR)-mediated signaling have been implicated in tumor cell invasion, ... ...

    Abstract The invasive ability of tumor cells plays a key role in prostate cancer metastasis and is a major cause of treatment failure. Urokinase plasminogen activator-(uPA) and its receptor (uPAR)-mediated signaling have been implicated in tumor cell invasion, survival, and metastasis in a variety of cancers. This study was undertaken to investigate the biological roles of uPA and uPAR in prostate cancer cell invasion and survival, and the potential of uPA and uPAR as targets for prostate cancer therapy. uPA and uPAR expression correlates with the metastatic potential of prostate cancer cells. Thus, therapies designed to inhibit uPA and uPAR expression would be beneficial. LNCaP, DU145, and PC3 are prostate cancer cell lines with low, moderate, and high metastatic potential, respectively, as demonstrated by their capacity to invade the extracellular matrix. In this study we utilized small hairpin RNAs (shRNAs), also referred to as small interfering RNAs, to target human uPA and uPAR. These small interfering RNA constructs significantly inhibited uPA and uPAR expression at both the mRNA and protein levels in the highly metastatic prostate cancer cell line PC3. Our data demonstrated that uPA-uPAR knockdown in PC3 cells resulted in a dramatic reduction of tumor cell invasion as indicated by a Matrigel invasion assay. Furthermore, simultaneous silencing of the genes for uPA and uPAR using a single plasmid construct expressing shRNAs for both uPA and uPAR significantly reduced cell viability and ultimately resulted in the induction of apoptotic cell death. RNA interference for uPA and uPAR also abrogated uPA-uPAR signaling to downstream target molecules such as ERK1/2 and Stat 3. In addition, our results demonstrated that intratumoral injection with the plasmid construct expressing shRNAs for uPA and uPAR almost completely inhibited established tumor growth and survival in an orthotopic mouse prostate cancer model. These findings uncovered evidence of a complex signaling network operating downstream of uPA-uPAR that actively advances tumor cell invasion, proliferation, and survival of prostate cancer cells. Thus, RNA interference-directed targeting of uPA and uPAR is a convenient and novel tool for studying the biological role of the uPA-uPAR system and raises the potential of its application for prostate cancer therapy.
    MeSH term(s) Animals ; Apoptosis ; Cell Line, Tumor ; Cell Proliferation ; Cell Survival ; Collagen/chemistry ; Collagen/pharmacology ; Drug Combinations ; Electrophoresis, Polyacrylamide Gel ; Extracellular Matrix/metabolism ; Gene Silencing ; Humans ; Immunoblotting ; Laminin/chemistry ; Laminin/pharmacology ; Male ; Mice ; Mice, Nude ; Microscopy, Fluorescence ; Mitogen-Activated Protein Kinase 1/metabolism ; Mitogen-Activated Protein Kinase 3/metabolism ; Neoplasm Invasiveness ; Neoplasm Metastasis ; Neoplasm Transplantation ; Neoplasms/pathology ; Plasmids/metabolism ; Prostatic Neoplasms/metabolism ; Prostatic Neoplasms/pathology ; Proteoglycans/chemistry ; Proteoglycans/pharmacology ; RNA Interference ; RNA, Small Interfering/metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; Signal Transduction ; Tetrazolium Salts/pharmacology ; Thiazoles/pharmacology ; Time Factors ; Transfection ; Urokinase-Type Plasminogen Activator/genetics ; Urokinase-Type Plasminogen Activator/metabolism
    Chemical Substances Drug Combinations ; Laminin ; Proteoglycans ; RNA, Small Interfering ; Tetrazolium Salts ; Thiazoles ; matrigel (119978-18-6) ; Collagen (9007-34-5) ; Mitogen-Activated Protein Kinase 1 (EC 2.7.11.24) ; Mitogen-Activated Protein Kinase 3 (EC 2.7.11.24) ; Urokinase-Type Plasminogen Activator (EC 3.4.21.73) ; thiazolyl blue (EUY85H477I)
    Language English
    Publishing date 2005-08-26
    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, P.H.S. ; Retracted Publication
    ZDB-ID 2997-x
    ISSN 1083-351X ; 0021-9258
    ISSN (online) 1083-351X
    ISSN 0021-9258
    DOI 10.1074/jbc.M503111200
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article: uPA/uPAR downregulation inhibits radiation-induced migration, invasion and angiogenesis in IOMM-Lee meningioma cells and decreases tumor growth in vivo.

    Kargiotis, Odysseas / Chetty, Chandramu / Gogineni, Venkateswara / Gondi, Christopher S / Pulukuri, Sai Muralikrishna / Kyritsis, Athanassios P / Gujrati, Meena / Klopfenstein, Jeffrey D / Dinh, Dzung H / Rao, Jasti S

    International journal of oncology

    2008  Volume 33, Issue 5, Page(s) 937–947

    Abstract: Meningioma is a well-known tumor of the central nervous system, and is treated by surgical resection and/or radiation. Recently, ionizing radiation has been shown to enhance invasiveness of surviving tumor cells, and several proteolytic enzyme molecules, ...

    Abstract Meningioma is a well-known tumor of the central nervous system, and is treated by surgical resection and/or radiation. Recently, ionizing radiation has been shown to enhance invasiveness of surviving tumor cells, and several proteolytic enzyme molecules, including urokinase plasminogen activator (uPA), seem to be upregulated after radiation. uPA and its receptor (uPAR) have been strongly implicated in tumor invasion, angiogenesis and progression. Hence, the tumor-associated uPA-uPAR system is considered a potential target for cancer therapy. In the present study, we show that radiation increases uPA levels in the IOMM-Lee meningioma cells, and subsequently, increases tumor invasion, migration and angiogenesis in vitro. Studies with signaling molecule inhibitors AG1478, U0126 and SB203580 (specific inhibitors of EGFR, MEK1/2 and p38 respectively) showed inhibition of uPA levels in both basal and irradiated-IOMM-Lee cells. The PI3K inhibitor (LY294002) and the AKT inhibitor (AKT inhibitor IV) also partially decreased uPA expression, whereas SP600125, a JNK inhibitor, did not affect uPA levels in either radiated or non-radiated cells. Further, a bicistronic plasmid construct with small interfering RNA (siRNA) against uPA and its receptor inhibited tumor invasion, migration and angiogenesis in radiation-treated IOMM-Lee cells. In addition, siRNA against uPA and its receptor inhibited subcutaneous tumor growth in athymic nude mice in combination with radiation in a synergistic manner. Thus, the specific targeting of proteases via RNA interference could augment the therapeutic effect of radiation and prevent the adverse effects resulting from tumor cells that receive sublethal doses of radiation within the tumor mass.
    MeSH term(s) Animals ; Capillaries/enzymology ; Capillaries/radiation effects ; Cell Line, Tumor ; Cell Movement/drug effects ; Cell Movement/radiation effects ; Cell Proliferation/drug effects ; Cell Proliferation/radiation effects ; Down-Regulation ; Extracellular Signal-Regulated MAP Kinases/antagonists & inhibitors ; Extracellular Signal-Regulated MAP Kinases/metabolism ; Female ; Genetic Therapy/methods ; Humans ; Meningeal Neoplasms/enzymology ; Meningeal Neoplasms/pathology ; Meningeal Neoplasms/radiotherapy ; Meningeal Neoplasms/therapy ; Meningioma/enzymology ; Meningioma/pathology ; Meningioma/radiotherapy ; Meningioma/therapy ; Mice ; Mice, Nude ; Neoplasm Invasiveness ; Neovascularization, Pathologic/enzymology ; Neovascularization, Pathologic/prevention & control ; Protein Kinase Inhibitors/pharmacology ; RNA Interference ; RNA, Small Interfering/metabolism ; Radiotherapy/adverse effects ; Receptor, Epidermal Growth Factor/antagonists & inhibitors ; Receptor, Epidermal Growth Factor/metabolism ; Receptors, Urokinase Plasminogen Activator/genetics ; Receptors, Urokinase Plasminogen Activator/metabolism ; Transfection ; Urokinase-Type Plasminogen Activator/genetics ; Urokinase-Type Plasminogen Activator/metabolism ; p38 Mitogen-Activated Protein Kinases/antagonists & inhibitors ; p38 Mitogen-Activated Protein Kinases/metabolism
    Chemical Substances Protein Kinase Inhibitors ; RNA, Small Interfering ; Receptors, Urokinase Plasminogen Activator ; EGFR protein, human (EC 2.7.10.1) ; Receptor, Epidermal Growth Factor (EC 2.7.10.1) ; Extracellular Signal-Regulated MAP Kinases (EC 2.7.11.24) ; p38 Mitogen-Activated Protein Kinases (EC 2.7.11.24) ; Urokinase-Type Plasminogen Activator (EC 3.4.21.73)
    Language English
    Publishing date 2008-11
    Publishing country Greece
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 1154403-x
    ISSN 1019-6439
    ISSN 1019-6439
    Database MEDical Literature Analysis and Retrieval System OnLINE

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