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      1. Author :
        Zhang, H; Fagan, D H; Zeng, X; Freeman, K T; Sachdev, D; Yee, D
      2. Title :
        Inhibition of cancer cell proliferation and metastasis by insulin receptor downregulation
      3. Type :
        Journal Article
      4. Year :
        2010
      5. Publication :
        Oncogene
      6. Products :

        Bioware cell lines

      7. Volume :
        29
      8. Issue :
        17
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        Animals; Bioware; Cell Line, Tumor; Cell Proliferation; Female; Humans; Insulin; Lung Neoplasms; Lymphangiogenesis; MDA-MB-231-D3H1 cells; Mice; Neoplasm Metastasis; Neoplasms, Experimental; Neovascularization, Pathologic; Phosphorylation; Proto-Oncogene Proteins c-akt; Receptor, Insulin; RNA, Small Interfering; Vascular Endothelial Growth Factor A
      12. Abstract :
        Insulin receptor (IR) and the type I IGF receptor (IGF1R) are structurally and functionally related. The function of IGF1R in cancer has been well documented and anti-IGF1R strategies to treat cancer have shown initial positive results. However, the role of IR in tumor biology, independent of IGF1R, is less clear. To address this issue, short hairpin RNA (shRNA) was used to specifically downregulate IR in two cancer cell lines, LCC6 and T47D. Cells with reduced IR showed reduced insulin-stimulated Akt activation, without affecting IGF1R activation. Cells with reduced IR formed fewer colonies in anchorage-independent conditions. LCC6 IR shRNA xenograft tumors in mice had reduced growth, angiogenesis and lymphangiogensis when compared with LCC6 wild-type cells. Accordingly, LCC6 IR shRNA clones produced less hypoxia-inducible factor-1alpha, vascular endothelial growth factor (VEGF)-A and VEGF-D. Furthermore, LCC6 IR shRNA cells formed fewer pulmonary metastases when compared with LCC6 wild-type cells. Using in vivo luciferase imaging, we have shown that LCC6 IR shRNA cells have less seeding and colonization potential in the lung and liver of mice than LCC6 cells. In conclusion, downregulation of IR inhibited cancer cell proliferation, angiogenesis, lymphangiogenesis and metastasis. Our data argue that IR should also be targeted in cancer therapy.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/20154728
      14. Call Number :
        PKI @ catherine.lautenschlager @
      15. Serial :
        8986
      1. Author :
        Zhang, J.; Preda, D. V.; Vasquez, K. O.; Morin, J.; Delaney, J.; Bao, B.; Percival, M. D.; Xu, D.; McKay, D.; Klimas, M.; Bednar, B.; Sur, C.; Gao, D. Z.; Madden, K.; Yared, W.; Rajopadhye, M.; Peterson, J. D.
      2. Title :
        A fluorogenic near-infrared imaging agent for quantifying plasma and local tissue renin activity in vivo and ex vivo
      3. Type :
        Journal Article
      4. Year :
        2012
      5. Publication :
        Am J Physiol Renal Physiol
      6. Products :

        ReninSense FASTFMT Imaging Systems

      7. Volume :
        303
      8. Issue :
        N/A
      9. Page Numbers :
        F593-603
      10. Research Area :
        N/A
      11. Keywords :
        ReninSense 680 FAST, FMT, Animal Feed/analysis; Animals; Cathepsin D; Cathepsin G; Female; Fluorescent Dyes/*pharmacology; Humans; Mice; Mice, Inbred C57BL; Peptides/*pharmacology; Peptidyl-Dipeptidase A/metabolism; Rats; Renin/*blood/*metabolism; Renin-Angiotensin System/physiology; Sensitivity and Specificity; Sodium, Dietary
      12. Abstract :
        The renin-angiotensin system (RAS) is well studied for its regulation of blood pressure and fluid homeostasis, as well as for increased activity associated with a variety of diseases and conditions, including cardiovascular disease, diabetes, and kidney disease. The enzyme renin cleaves angiotensinogen to form angiotensin I (ANG I), which is further cleaved by angiotensin-converting enzyme to produce ANG II. Although ANG II is the main effector molecule of the RAS, renin is the rate-limiting enzyme, thus playing a pivotal role in regulating RAS activity in hypertension and organ injury processes. Our objective was to develop a near-infrared fluorescent (NIRF) renin-imaging agent for noninvasive in vivo detection of renin activity as a measure of tissue RAS and in vitro plasma renin activity. We synthesized a renin-activatable agent, ReninSense 680 FAST (ReninSense), using a NIRF-quenched substrate derived from angiotensinogen that is cleaved specifically by purified mouse and rat renin enzymes to generate a fluorescent signal. This agent was assessed in vitro, in vivo, and ex vivo to detect and quantify increases in plasma and kidney renin activity in sodium-sensitive inbred C57BL/6 mice maintained on a low dietary sodium and diuretic regimen. Noninvasive in vivo fluorescence molecular tomographic imaging of the ReninSense signal in the kidney detected increased renin activity in the kidneys of hyperreninemic C57BL/6 mice. The agent also effectively detected renin activity in ex vivo kidneys, kidney tissue sections, and plasma samples. This approach could provide a new tool for assessing disorders linked to altered tissue and plasma renin activity and to monitor the efficacy of therapeutic treatments.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/22674025
      14. Call Number :
        PKI @ kd.modi @ 1
      15. Serial :
        10572
      1. Author :
        Zhang, X.; Bloch, S.; Akers, W.; Achilefu, S.
      2. Title :
        Near-infrared molecular probes for in vivo imaging
      3. Type :
        Journal Article
      4. Year :
        2012
      5. Publication :
        Curr Protoc Cytom
      6. Products :

        IntegriSense

      7. Volume :
        Chapter 12
      8. Issue :
        N/A
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        IntegriSense, Animals; Cell Line, Tumor; Diagnostic Imaging/*methods; Fluorescent Dyes/chemistry/metabolism; Humans; Mice; Molecular Probes/*diagnostic use; Nanoparticles/chemistry; Quantum Dots; Spectroscopy, Near-Infrared/*methods
      12. Abstract :
        Cellular and tissue imaging in the near-infrared (NIR) wavelengths between 700 and 900 nm is advantageous for in vivo imaging because of the low absorption of biological molecules in this region. This unit presents protocols for small animal imaging using planar and fluorescence lifetime imaging techniques. Included is an overview of NIR fluorescence imaging of cells and small animals using NIR organic fluorophores, nanoparticles, and multimodal imaging probes. The development, advantages, and application of NIR fluorescent probes that have been used for in vivo imaging are also summarized. The use of NIR agents in conjunction with visible dyes and considerations in selecting imaging agents are discussed. We conclude with practical considerations for the use of these dyes in cell and small animal imaging applications.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/22470154
      14. Call Number :
        PKI @ kd.modi @ 24
      15. Serial :
        10386
      1. Author :
        Zhang, Z.; Hu, Z.; Gupta, J.; Krimmel, J. D.; Gerseny, H. M.; Berg, A. F.; Robbins, J. S.; Du, H.; Prabhakar, B.; Seth, P.
      2. Title :
        Intravenous administration of adenoviruses targeting transforming growth factor beta signaling inhibits established bone metastases in 4T1 mouse mammary tumor model in an immunocompetent syngeneic host
      3. Type :
        Journal Article
      4. Year :
        2012
      5. Publication :
        Cancer Gene Ther
      6. Products :

        Bioware cell linesIVIS Imaging Systems

      7. Volume :
        19
      8. Issue :
        N/A
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        4T1-luc2, IVIS, Bioluminescence, Adenoviridae/genetics/*metabolism/physiology; Administration, Intravenous; Animals; Bone Neoplasms/secondary/*therapy; Cell Line, Tumor; Female; Humans; Immunocompetence; Luminescent Measurements/methods; Mammary Neoplasms, Experimental/pathology/*therapy; Mice; Mice, Inbred BALB C; Oncolytic Virotherapy/methods; Oncolytic Viruses/genetics/metabolism/physiology; Phosphorylation; Promoter Regions, Genetic; Protein-Serine-Threonine Kinases/genetics/*metabolism; Receptors, Transforming Growth Factor beta/genetics/*metabolism; Signal Transduction; Smad2 Protein/genetics/metabolism; Telomerase/genetics; Transforming Growth Factor beta1/genetics/metabolism; Transplantation, Isogeneic/methods; Tumor Stem Cell Assay/methods; Virus Replication
      12. Abstract :
        We have examined the effect of adenoviruses expressing soluble transforming growth factor receptorII-Fc (sTGFbetaRIIFc) in a 4T1 mouse mammary tumor bone metastasis model using syngeneic BALB/c mice. Infection of 4T1 cells with a non-replicating adenovirus, Ad(E1-).sTbetaRFc, or with two oncolytic adenoviruses, Ad.sTbetaRFc and TAd.sTbetaRFc, expressing sTGFbetaRIIFc (the human TERT promoter drives viral replication in TAd.sTbetaRFc) produced sTGFbetaRIIFc protein. Oncolytic adenoviruses produced viral replication and induced cytotoxicity in 4T1 cells. 4T1 cells were resistant to the cytotoxic effects of TGFbeta-1 (up to 10 ng ml(-1)). However, TGFbeta-1 induced the phosphorylation of SMAD2 and SMAD3, which were inhibited by co-incubation with sTGFbetaRIIFc protein. TGFbeta-1 also induced interleukin-11, a well-known osteolytic factor. Intracardiac injection of 4T1-luc2 cells produced bone metastases by day 4. Intravenous injection of Ad.sTbetaRFc (on days 5 and 7) followed by bioluminescence imaging (BLI) of mice on days 7, 11 and 14 in tumor-bearing mice indicated inhibition of bone metastasis progression (P<0.05). X-ray radiography of mice on day 14 showed a significant reduction of the lesion size by Ad.sTbetaRFc (P<0.01) and TAd.sTbetaRFc (P<0.05). Replication-deficient virus Ad(E1-).sTbetaRFc expressing sTGFbetaRIIFc showed some inhibition of bone metastasis, whereas Ad(E1-).Null was not effective in inhibiting bone metastases. Thus, systemic administration of Ad.sTbetaRFc and TAd.sTbetaRFc can inhibit bone metastasis in the 4T1 mouse mammary tumor model, and can be developed as potential anti-tumor agents for breast cancer.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/22744210
      14. Call Number :
        PKI @ kd.modi @ 7
      15. Serial :
        10479
      1. Author :
        Zhou, H.; Roy, S.; Cochran, E.; Zouaoui, R.; Chu, C. L.; Duffner, J.; Zhao, G.; Smith, S.; Galcheva-Gargova, Z.; Karlgren, J.; Dussault, N.; Kwan, R. Y.; Moy, E.; Barnes, M.; Long, A.; Honan, C.; Qi, Y. W.; Shriver, Z.; Ganguly, T.; Schultes, B.; Venkataraman, G.; Kishimoto, T. K.
      2. Title :
        M402, a novel heparan sulfate mimetic, targets multiple pathways implicated in tumor progression and metastasis
      3. Type :
        Journal Article
      4. Year :
        2011
      5. Publication :
        PLoS One
      6. Products :

        Bioware cell lines

      7. Volume :
        6
      8. Issue :
        N/A
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        IVIS, 4T1-luc2
      12. Abstract :
        Heparan sulfate proteoglycans (HSPGs) play a key role in shaping the tumor microenvironment by presenting growth factors, cytokines, and other soluble factors that are critical for host cell recruitment and activation, as well as promoting tumor progression, metastasis, and survival. M402 is a rationally engineered, non-cytotoxic heparan sulfate (HS) mimetic, designed to inhibit multiple factors implicated in tumor-host cell interactions, including VEGF, FGF2, SDF-1alpha, P-selectin, and heparanase. A single s.c. dose of M402 effectively inhibited seeding of B16F10 murine melanoma cells to the lung in an experimental metastasis model. Fluorescent-labeled M402 demonstrated selective accumulation in the primary tumor. Immunohistological analyses of the primary tumor revealed a decrease in microvessel density in M402 treated animals, suggesting anti-angiogenesis to be one of the mechanisms involved in-vivo. M402 treatment also normalized circulating levels of myeloid derived suppressor cells in tumor bearing mice. Chronic administration of M402, alone or in combination with cisplatin or docetaxel, inhibited spontaneous metastasis and prolonged survival in an orthotopic 4T1 murine mammary carcinoma model. These data demonstrate that modulating HSPG biology represents a novel approach to target multiple factors involved in tumor progression and metastasis.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/21698156
      14. Call Number :
        PKI @ kd.modi @ 1
      15. Serial :
        10362
      1. Author :
        Zhuang, H.; Jiang, W.; Zhang, X.; Qiu, F.; Gan, Z.; Cheng, W.; Zhang, J.; Guan, S.; Tang, B.; Huang, Q.; Wu, X.; Huang, X.; Hu, Q.; Lu, M.; Hua, Z. C.
      2. Title :
        Suppression of HSP70 expression sensitizes NSCLC cell lines to TRAIL-induced apoptosis by upregulating DR4 and DR5 and downregulating c-FLIP-L expressions
      3. Type :
        Journal Article
      4. Year :
        2012
      5. Publication :
        J Mol Med (Berl)
      6. Products :

        Bioware cell linesIVIS Imaging Systems

      7. Volume :
        N/A
      8. Issue :
        N/A
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        A549-luc-C8, A549-luc, IVIS, Bioware
      12. Abstract :
        Many cancer cell types are resistant to tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced apoptosis. Here, we examined whether HSP70 suppression by small interfering RNA (siRNA) sensitized non-small cell lung cancer (NSCLC) cells to TRAIL-induced apoptosis and the underlying mechanisms. We demonstrated that HSP70 suppression by siRNA sensitized NSCLC cells to TRAIL-induced apoptosis by upregulating the expressions of death receptor 4 (DR4) and death receptor 5 (DR5) through activating NF-kappaB, JNK, and, subsequently, p53, consequently significantly amplifying TRAIL-mediated caspase-8 processing and activity, cytosolic translocation of cytochrome c, and cell death. Consistently, the pro-apoptotic proteins Bad and Bax were upregulated, while the anti-apoptotic protein Bcl-2 was downregulated. The luciferase activity of the DR4 promoter was blocked by a NF-kappaB pathway inhibitor BAY11-7082, suggesting that NF-kappaB activation plays an important role in the transcriptional upregulation of DR4. Additionally, HSP70 suppression inhibited the phosphorylation of ERK, AKT, and PKC, thereby downregulating c-FLIP-L. A549 xenografts in mice receiving HSP70 siRNA showed TRAIL-induced cell death and increased DR4/DR5 levels and reduced tumor growth. The combination of psiHSP70 gene therapy with TRAIL also significantly increased the survival benefits induced by TRAIL therapy alone. Interestingly, HSP27 siRNA and TRAIL together could not suppress tumor growth or prolong the survival of tumor-bearing mice significantly, although the combination could efficiently induce the apoptosis of A549 cells in vitro. Our findings suggest that HSP70 suppression or downregulation might be promising to overcome TRAIL resistance in cancer.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/22948392
      14. Call Number :
        PKI @ kd.modi @ 2
      15. Serial :
        10526
      1. Author :
        Zollo, M.; Di Dato, V.; Spano, D.; De Martino, D.; Liguori, L.; Marino, N.; Vastolo, V.; Navas, L.; Garrone, B.; Mangano, G.; Biondi, G.; Guglielmotti, A.
      2. Title :
        Targeting monocyte chemotactic protein-1 synthesis with bindarit induces tumor regression in prostate and breast cancer animal models
      3. Type :
        Journal Article
      4. Year :
        2012
      5. Publication :
        Clin Exp Metastasis
      6. Products :

        Bioware cell linesIVIS Imaging Systems

      7. Volume :
        29
      8. Issue :
        N/A
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        PC-3M-luc2, PC3M-luc2, IVIS, Prostate Cancer, Bioware, Animals; Breast Neoplasms/*pathology; Cell Line, Tumor; Cell Movement; Cell Proliferation; Chemokine CCL2/*biosynthesis/chemistry/metabolism; Female; Humans; Indazoles/*pharmacology; Macrophages/metabolism; Male; Mice; Mice, Inbred BALB C; NF-kappa B/metabolism; Neoplasm Metastasis; Neoplasm Transplantation; Propionates/*pharmacology; Prostatic Neoplasms/*pathology; Signal Transduction
      12. Abstract :
        Prostate and breast cancer are major causes of death worldwide, mainly due to patient relapse upon disease recurrence through formation of metastases. Chemokines are small proteins with crucial roles in the immune system, and their regulation is finely tuned in early inflammatory responses. They are key molecules during inflammatory processes, and many studies are focusing on their regulatory functions in tumor growth and angiogenesis during metastatic cell seeding and spreading. Bindarit is an anti-inflammatory indazolic derivative that can inhibit the synthesis of MCP-1/CCL2, with a potential inhibitory function in tumor progression and metastasis formation. We show here that in vitro, bindarit can modulate cancer-cell proliferation and migration, mainly through negative regulation of TGF-beta and AKT signaling, and it can impair the NF-kappaB signaling pathway through enhancing the expression of the NF-kappaB inhibitor IkB-alpha. In vivo administration of bindarit results in impaired metastatic disease in prostate cancer xenograft mice (PC-3M-Luc2 cells injected intra-cardially) and impairment of local tumorigenesis in syngeneic Balb/c mice injected under the mammary gland with murine breast cancer cells (4T1-Luc cells). In addition, bindarit treatment significantly decreases the infiltration of tumor-associated macrophages and myeloid-derived suppressor cells in 4T1-Luc primary tumors. Overall, our data indicate that bindarit is a good candidate for new therapies against prostate and breast tumorigenesis, with an action through impairment of inflammatory cell responses during formation of the tumor-stroma niche microenvironment.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/22484917
      14. Call Number :
        PKI @ kd.modi @ 6
      15. Serial :
        10489
      1. Author :
        Zongjin Li, Kitchener D. Wilson, Bryan Smith, Daniel L. Kraft, Fangjun Jia, Mei Huang, Xiaoyan Xie, Robert C. Robbins, Sanjiv S. Gambhir, Irving L. Weissman and Joseph C. Wu
      2. Title :
        Functional and Transcriptional Characterization of Human Embryonic Stem Cell-Derived Endothelial Cells for Treatment of Myocardial Infarction
      3. Type :
        Journal Article
      4. Year :
        2009
      5. Publication :
        PLoS One
      6. Products :

        AngioSense

      7. Volume :
        4
      8. Issue :
        12
      9. Page Numbers :
        N/A
      10. Research Area :
        Cardiovascular Research
      11. Keywords :
        in vivo imaging; human embryonic stem cells; hESCs; endothelial cells; ECs; AngioSense
      12. Abstract :
        Background: Differentiation of human embryonic stem cells into endothelial cells (hESC-ECs) has the potential to provide an unlimited source of cells for novel transplantation therapies of ischemic diseases by supporting angiogenesis and vasculogenesis. However, the endothelial differentiation efficiency of the conventional embryoid body (EB) method is low while the 2-dimensional method of co-culturing with mouse embryonic fibroblasts (MEFs) require animal product, both of which can limit the future clinical application of hESC-ECs. Moreover, to fully understand the beneficial effects of stem cell therapy, investigators must be able to track the functional biology and physiology of transplanted cells in living subjects over time.

        Methodology: In this study, we developed an extracellular matrix (ECM) culture system for increasing endothelial differentiation and free from contaminating animal cells. We investigated the transcriptional changes that occur during endothelial differentiation of hESCs using whole genome microarray, and compared to human umbilical vein endothelial cells (HUVECs). We also showed functional vascular formation by hESC-ECs in a mouse dorsal window model. Moreover, our study is the first so far to transplant hESC-ECs in a myocardial infarction model and monitor cell fate using molecular imaging methods.

        Conclusion: Taken together, we report a more efficient method for derivation of hESC-ECs that express appropriate patterns of endothelial genes, form functional vessels in vivo, and improve cardiac function. These studies suggest that hESC-ECs may provide a novel therapy for ischemic heart disease in the future.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2795856/?tool=pubmed
      14. Call Number :
        PKI @ sarah.piper @
      15. Serial :
        4557
      1. Author :
        Zuluaga, M. F.; Sekkat, N.; Gabriel, D.; van den Bergh, H.; Lange, N.
      2. Title :
        Selective Photodetection and Photodynamic Therapy of Prostate Cancer through Targeting of Proteolytic Activity
      3. Type :
        Journal Article
      4. Year :
        2012
      5. Publication :
        Mol Cancer Ther
      6. Products :

        Bioware cell linesIVIS Imaging Systems

      7. Volume :
        N/A
      8. Issue :
        N/A
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        PC-3M-luc-C6, PC-3M-luc, IVIS, Bioware, Prostate cancer, Bioluminescence
      12. Abstract :
        Frequent side effects of radical treatment modalities and the availability of novel diagnostics have raised the interest in focal therapies for localized prostate cancer. To improve the selectivity and therapeutic efficacy of such therapies, we developed a minimally invasive procedure, based on a novel polymeric photosensitizer prodrug sensitive to urokinase-like plasminogen activator (uPA). The compound is inactive in its prodrug form and accumulates passively at the tumor site by the enhanced permeability and retention effect. There, the prodrug is selectively converted to its photoactive form by uPA which is over-expressed by prostate cancer cells. Irradiation of the activated photosensitizer exerts a tumor-selective phototoxic effect. The prodrug alone (8 microM) showed no toxic effect on PC-3 cells, but upon irradiation the cell viability was reduced by 90%. In vivo, after systemic administration of the prodrug, PC-3 xenografts became selectively fluorescent. This is indicative of the prodrug accumulation in the tumor and selective local enzymatic activation. Qualitative analysis of the activated compound confirmed that the enzymatic cleavage occurred selectively in the tumor, with only trace amounts in the neighboring skin or muscle. Subsequent photodynamic therapy studies demonstrated complete tumor eradication of animals treated with light (150 J/cm2 at 665 nm) 16 hours after the injection of the prodrug (7.5 mg/kg). These promising results evidence the excellent selectivity of our prodrug with the potential to be used for both, imaging and therapy of localized prostate cancer.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/23270928
      14. Call Number :
        PKI @ kd.modi @ 5
      15. Serial :
        10542
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[31–40] << < Back 41 42 43 44 45 46 47 48 49 50 Next >     List View  | Details print