11 results on '"Liu, Jian-Miao"'
Search Results
2. Cyclin K and cyclin D1b are oncogenic in myeloma cells
- Author
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Renoir Jack-Michel, Wdzieczak-Bakala Joanna, Jost Bernard, Dembele Doulaye, Liu Jian-Miao, Andrieux Geoffroy, Tchakarska Guergana, Marsaud Véronique, and Sola Brigitte
- Subjects
Neoplasms. Tumors. Oncology. Including cancer and carcinogens ,RC254-282 - Abstract
Abstract Background Aberrant expression of cyclin D1 is a common feature in multiple myeloma (MM) and always associated with mantle cell lymphoma (MCL). CCND1 gene is alternatively spliced to produce two cyclin D1 mRNA isoforms which are translated in two proteins: cyclin D1a and cyclin D1b. Both isoforms are present in MM cell lines and primary cells but their relative role in the tumorigenic process is still elusive. Results To test the tumorigenic potential of cyclin D1b in vivo, we generated cell clones derived from the non-CCND1 expressing MM LP-1 cell line, synthesizing either cyclin D1b or cyclin K, a structural homolog and viral oncogenic form of cyclin D1a. Immunocompromised mice injected s.c. with LP-1K or LP-1D1b cells develop tumors at the site of injection. Genome-wide analysis of LP-1-derived cells indicated that several cellular processes were altered by cyclin D1b and/or cyclin K expression such as cell metabolism, signal transduction, regulation of transcription and translation. Importantly, cyclin K and cyclin D1b have no major action on cell cycle or apoptosis regulatory genes. Moreover, they impact differently cell functions. Cyclin K-expressing cells have lost their migration properties and display enhanced clonogenic capacities. Cyclin D1b promotes tumorigenesis through the stimulation of angiogenesis. Conclusions Our study indicates that cyclin D1b participates into MM pathogenesis via previously unrevealed actions.
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- 2010
- Full Text
- View/download PDF
3. A novel iodomethylene-dimethyl-dihydropyranone induces G2/M arrest and apoptosis in human cancer cells
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Bignon, Jérôme, Bénéchie, Michel, Herlem, Denyse, Liu, Jian-Miao, Pinault, Alexia, Khuong-Huu, Françoise, Wdzieczak-Bakala, Joanna, Institut de Chimie des Substances Naturelles (ICSN), and Centre National de la Recherche Scientifique (CNRS)-Institut de Chimie du CNRS (INC)
- Subjects
G2 Phase ,Molecular Structure ,Pyrones ,Neoplasms ,Tumor Cells, Cultured ,Humans ,Antineoplastic Agents ,Apoptosis ,[SDV.BC]Life Sciences [q-bio]/Cellular Biology ,Cell Division - Abstract
International audience; BACKGROUND: The putative pharmacophore of a naturally cytotoxic limonoid haperforin B1, E-5-iodomethylene-6,6-dimethyl-5,6-dihydropyran-2-one (IDDP) was synthesized and its biological activity was investigated. MATERIALS AND METHODS: The cytotoxicity of IDDP was assessed using human breast, lung, colorectal and epidermal carcinomas, chronic myeloid leukemia and glioblastoma cell lines. Cell cycle analysis was performed by flow cytometry. The induction of apoptosis was studied by a caspase assay and by annexin V-propidium iodide double staining. The organization of actin and tubulin microfilaments was analysed by immunocytochemical labeling. RESULTS: IDDP was shown to inhibit the growth of a panel of human cancer cell lines independently of their p53 status with IC(50) ranging from 0.07 to 0.50 muM. All the treated cells were arrested in the G(2)/M phase in a time-dependent manner before cell death occurred through an apoptotic pathway. Immunocytochemical studies revealed that the normal organization of microfilaments and microtubules was disrupted in IDDP exposed cells. CONCLUSION: IDDP can be considered as a promising anticancer agent.
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- 2009
4. Overexpression of the Angiogenic Tetrapeptide AcSDKP in Human Malignant Tumors
- Author
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Liu, Jian-Miao and Liu, Jian-Miao
- Abstract
Background: The natural tetrapeptide acetyl-SerAsp-Lys-Pro (AcSDKP), generated from thymosin beta 4 following its cleavage by prolyl oligopeptidase (POP), is a physiological stimulator of angiogenesis. Because of the critical role of neovascularisation in tumor development, the expression of AcSDKP and the activity of POP were examined in different human solid malignancies. Materials and Methods: The expression of AcSDKP and the activity of POP were evaluated in human blood samples and tissue specimens of thyroid goiter and thyroid papillary carcinoma as well as in commercial cancer tissue microarray. Results: A significantly increased concentration of AcSDKP in intratumoral blood and enhanced tissular activity of POP were detected in cancer patients. The expression of AcSDKP in human breast, colon, head and neck, kidney, lung, skin, ovary and prostate cancer tissues was shown to be greater than that in normal tissues. Conclusion: AcSDKP and POP contribute to the malignant phenotype and these molecules are potentiel markers of cancer.
- Published
- 2008
5. Evidence for an association of high levels of endogenous Acetyl-Ser-Asp-Lys-Pro, a potent mediator of angiogenesis, with acute myeloid leukemia development
- Author
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Liu, Jian-Miao and Liu, Jian-Miao
- Abstract
Evidence from clinical and laboratory studies suggests that angiogenesis is important in the progression of solid tumours and hematologic malignancies. We have shown that the naturally occurring tetrapeptide Acetyl-Ser-Asp-Lys-Pro (AcSDKP) is a potent angiogenic factor normally present at nanomolar concentrations in the blood. A murine leukemia model was used to assess whether there was a correlation between levels of endogenous AcSDKP and the development of disease. Levels of AcSDKP in the plasma and bone marrow (BM) cells from mice bearing an acute myeloid leukemia (AML) were five- to ten-fold greater than those in non-leukemic mice. Furthermore, a strong correlation between the concentration of endogenous AcSDKP and the progression of AML was demonstrated. These results are consistent with the marked increase in BM vascularity observed in leukemic mice. The physiologic relevance of these findings awaits further studies and the contribution of AcSDKP to the pathogenesis of leukemia is under investigation.
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- 2006
6. Cyclin K and cyclin D1b are oncogenic in myeloma cells
- Author
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Marsaud, Véronique, primary, Tchakarska, Guergana, additional, Andrieux, Geoffroy, additional, Liu, Jian-Miao, additional, Dembele, Doulaye, additional, Jost, Bernard, additional, Wdzieczak-Bakala, Joanna, additional, Renoir, Jack-Michel, additional, and Sola, Brigitte, additional
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- 2010
- Full Text
- View/download PDF
7. Tetrapeptide AcSDKP Induces Postischemic Neovascularization Through Monocyte Chemoattractant Protein-1 Signaling
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Waeckel, Ludovic, primary, Bignon, Jérôme, additional, Liu, Jian-Miao, additional, Markovits, Delphine, additional, Ebrahimian, Téni G., additional, Vilar, José, additional, Mees, Barend, additional, Blanc-Brude, Olivier, additional, Barateau, Véronique, additional, Le ricousse-Roussanne, Sophie, additional, Duriez, Micheline, additional, Tobelem, Gérard, additional, Wdzieczak-Bakala, Joanna, additional, Lévy, Bernard I, additional, and Silvestre, Jean-Sébastien, additional
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- 2006
- Full Text
- View/download PDF
8. Overexpression of the angiogenic tetrapeptide AcSDKP in human malignant tumors
- Author
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Liu, Jian-Miao, Kusinski, Michal, Ilic, Vesna, Bignon, Jerome, Hajem, Neila, Komorowski, Jan, Kuzdak, Krzysztof, Henryk Stepien, Wdzieczak-Bakala, Joanna, Institut de Chimie des Substances Naturelles (ICSN), and Centre National de la Recherche Scientifique (CNRS)-Institut de Chimie du CNRS (INC)
- Subjects
marker ,angiogenesis ,genetic structures ,thyroid tumor ,[CHIM.ORGA]Chemical Sciences/Organic chemistry ,cancer ,POP ,AcSDKP ,ComputingMilieux_MISCELLANEOUS - Abstract
Background: The natural tetrapeptide acetyl-SerAsp-Lys-Pro (AcSDKP), generated from thymosin beta 4 following its cleavage by prolyl oligopeptidase (POP), is a physiological stimulator of angiogenesis. Because of the critical role of neovascularisation in tumor development, the expression of AcSDKP and the activity of POP were examined in different human solid malignancies. Materials and Methods: The expression of AcSDKP and the activity of POP were evaluated in human blood samples and tissue specimens of thyroid goiter and thyroid papillary carcinoma as well as in commercial cancer tissue microarray. Results: A significantly increased concentration of AcSDKP in intratumoral blood and enhanced tissular activity of POP were detected in cancer patients. The expression of AcSDKP in human breast, colon, head and neck, kidney, lung, skin, ovary and prostate cancer tissues was shown to be greater than that in normal tissues. Conclusion: AcSDKP and POP contribute to the malignant phenotype and these molecules are potentiel markers of cancer.
9. Overexpression of the angiogenic tetrapeptide AcSDKP in human malignant tumors.
- Author
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Liu JM, Kusinski M, Ilic V, Bignon J, Hajem N, Komorowski J, Kuzdak K, Stepien H, and Wdzieczak-Bakala J
- Subjects
- Adolescent, Adult, Aged, Carcinoma, Papillary blood, Carcinoma, Papillary enzymology, Carcinoma, Papillary metabolism, Female, Humans, Male, Middle Aged, Neoplasms blood, Neoplasms enzymology, Oligopeptides blood, Prolyl Oligopeptidases, Serine Endopeptidases metabolism, Thyroid Neoplasms blood, Thyroid Neoplasms enzymology, Thyroid Neoplasms metabolism, Young Adult, Neoplasms metabolism, Oligopeptides biosynthesis
- Abstract
Background: The natural tetrapeptide acetyl-Ser-Asp-Lys-Pro (AcSDKP), generated from thymosin beta4 following its cleavage by prolyl oligopeptidase (POP), is a physiological stimulator of angiogenesis. Because of the critical role of neovascularisation in tumor development, the expression of AcSDKP and the activity of POP were examined in different human solid malignancies., Materials and Methods: The expression of AcSDKP and the activity of POP were evaluated in human blood samples and tissue specimens of thyroid goiter and thyroid papillary carcinoma as well as in commercial cancer tissue microarray., Results: A significantly increased concentration of AcSDKP in intratumoral blood and enhanced tissular activity of POP were detected in cancer patients. The expression of AcSDKP in human breast, colon, head and neck, kidney, lung, skin, ovary and prostate cancer tissues was shown to be greater than that in normal tissues., Conclusion: AcSDKP and POP contribute to the malignant phenotype and these molecules are potentiel markers of cancer.
- Published
- 2008
10. Sodium phenylacetate (NaPa) improves the TAM effect on glioblastoma experimental tumors by inducing cell growth arrest and apoptosis.
- Author
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Wei MX, Liu JM, Gadal F, Yi P, Liu J, and Crepin M
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- Animals, Apoptosis drug effects, Brain Neoplasms pathology, Cell Growth Processes drug effects, Cell Line, Tumor, Drug Synergism, Female, Glioblastoma pathology, Gliosarcoma drug therapy, Gliosarcoma pathology, Mice, Mice, Nude, Phenylacetates administration & dosage, Rats, Tamoxifen administration & dosage, Antineoplastic Combined Chemotherapy Protocols pharmacology, Brain Neoplasms drug therapy, Glioblastoma drug therapy
- Abstract
Background: Multiform glioblastomas represent the most aggressive brain tumors. Here, the cooperative effects of sodium phenylacetate (NaPa) and/or tamoxifen (TAM) on CNS1 and 9L glioblastoma cell lines in vitro and in an experimental animal tumor model were investigated., Materials and Methods: The drug effects on cell cycle and apoptosis were investigated by flow cytometry. CNS1 cells were implanted subcutaneously in nude mice to form tumors which were then treated with NaPa, TAM or NaPa/TAM., Results: A significant inhibitory effect of NaPa on the two glioma cell lines (LD50 of 10 mM) was observed. 10(-5) M of TAM inhibited approximately 35% of 9L cell growth, and 90% of CNS1 cell growth. When a combination of both drugs included 10(-9) M of TAM, inhibition of about 50% of 9L cell growth and 75% of CNS1 cell growth occurred. The NaPa/TAM combined treatment increased the number of G0/G1 arrested cells and apoptotic cells as compared to treatments with NaPa or TAM alone. Inhibition of CNS1 tumor growth were observed after a two week treatment with NaPa (32 mg/kg/day) or TAM (6 mg/kg/day)., Conclusion: These results showed a synergistic effect between these two drugs on tumor cell proliferation, caused by cell cycle arrest in the G0/G1 phase and by induction of apoptosis.
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- 2007
11. Inhibitory effect of fucoidan on the adhesion of adenocarcinoma cells to fibronectin.
- Author
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Liu JM, Bignon J, Haroun-Bouhedja F, Bittoun P, Vassy J, Fermandjian S, Wdzieczak-Bakala J, and Boisson-Vidal C
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- Actins metabolism, Adenocarcinoma metabolism, Antineoplastic Agents metabolism, Breast Neoplasms metabolism, Cell Adhesion drug effects, Cell Line, Tumor, Cell Membrane metabolism, Cell Membrane pathology, Dose-Response Relationship, Drug, Extracellular Matrix metabolism, Extracellular Matrix pathology, Humans, Integrin alpha5 biosynthesis, Integrin beta1 biosynthesis, Polysaccharides metabolism, Adenocarcinoma pathology, Antineoplastic Agents pharmacology, Breast Neoplasms pathology, Fibronectins metabolism, Polysaccharides pharmacology
- Abstract
Fucoidans inhibit tumour cell adhesion to various substrata, but their mechanisms of action are not fully understood. Using 3H-fucoidan, we observed that fucoidan binds to fibronectin, this binding being saturable and sensitive to ionic strength and pH. The interaction occurred on at least four different sites along the polypeptide chain, two of them being the heparin-binding sequences. Moreover, when MDA-MB-231 tumour cells were exposed to DTAF-fucoidan, internalization occurred and punctuated vesicles were observed in the perinuclear region. The treated cells also showed a different morphology with a cytoskeleton devoid of vinculin and a reorganiztion of the repartition of the integrin-alpha5 subunit on the cell surface. Based on these data, we hypothesize that fucoidan inhibits the adhesion of MDA-MB-231 cells to fibronectin i) by blocking the protein's heparin- and cell-binding domains, ii) by modulating the reorganization of the integrin alpha5 subunit and iii) by down-regulating the expression of vinculin.
- Published
- 2005
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