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Molecular determinants of transforming growth factor beta-1 action on human glioblastoma cells ; Молекулярные детерминанты действия трансформирующего фактора роста бета-1 на клетки глиобластомы человека

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  • معلومة اضافية
    • بيانات النشر:
      “ABV-press” Publishing house”, LLC
    • الموضوع:
      2016
    • Collection:
      Advances in molecular oncology (E-Journal) / Успехи молекулярной онкологии
    • نبذة مختصرة :
      Background. Increased expression of transforming growth factor beta-1 (TGF-β1) in malignant brain tumors promotes cancer cells survival enhancing their growth, migration, invasion, angiogenesis, immune system suppression.Objective is to study molecular mechanisms of TGF-β1 action on U87 human glioblastoma cells by means of proteomic high-resolution massspectrometry.Results. We have identified intracell signal pathways responsible for TGF-β1 involvement in malignant gliomas oncogenesis including differential expressed proteins of tight cell junctions, focal adhesion, histone deacetylases, heat shock, S100 family.Conclusions. Important patterns are determined that could be used for the development of new approaches for detection of glioblastoma metastasis candidate markers and potential therapy targets of this decease. ; Введение. Повышенная экспрессия трансформирующего фактора роста бета-1 (transforming growth factor beta1 , TGF-β1) в злокачественных опухолях головного мозга способствует выживанию опухолевых клеток, увеличивая их рост, миграцию, инвазию, ангиогенез, супрессию иммунной системы.Цель работы – методом протеомной масс-спектрометрии высокого разрешения изучить молекулярные механизмы действия TGF-β1 на клетки U87 глиобластомы человека.Результаты. Идентифицированы внутриклеточные сигнальные пути, ответственные за участие TGF-β1 в онкогенезе злокачественных глиом и включающие дифференциально экспрессированные белки плотных межклеточных контактов, фокальной адгезии, деацелаз гистонов, теплового шока, семейства S100.Заключение. Установлены важные закономерности, которые могут быть использованы при разработке новых подходов для обнаружения кандидатных маркеров метастазирования глиобластомы и потенциальных мишеней для терапии этого заболевания.
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      application/pdf
    • Relation:
      https://umo.abvpress.ru/jour/article/view/62/63; Holland E. C. Glioblastoma multiforme: the terminator. Proc Natl Acad Sci USA 2000;97(12):6242–4.; Adamson C., Kanu O. O., Mehta A. I. et al. Glioblastoma multiforme: a review of where we have been and where we are going. Expert Opin Investig Drugs 2009;18(8):1061–83.; Wang Y., Jiang T. Understanding high grade glioma: molecular mechanism, therapy and comprehensive management. Cancer Lett 2013;331:139–46.; Westphal M., Lamszus K. The neurobiology of gliomas: from cell biology to the development of therapeutic approaches. Nat Rev Neurosci 2011;12(9):495–508.; Rich J. N. The role of transforming growth factor-beta in primary brain tumors. Front Biosci 2003;8:e245–60.; Gregory P. A., Bracken C. P., Smith E. et al. An autocrine TGF-beta/ZEB/miR-200 signaling network regulates establishment and maintenance of epithelial – mesenchymal transition. Mol Biol Cell 2011;22(10): 1686–98.; Seoane J. Escaping from the TGF-beta anti-proliferative control. Carcinogenesis 2006;27(11):2148–56.; Siegel P. M., Massague J. Cytostatic and apoptotic actions of TGF-beta in homeostasis and cancer. Nat Rev Cancer 2003;3(11): 807–21.; Rahimi R. A., Leof E. B. TGF-beta signaling: a tale of two responses. J Cell Biochem 2007;102(3):593–608.; Taube J. H., Herschkowitz J. I., Komurov K. et al. Core epithelial-to-mesenchymal transition interactome gene-expression signature is associated with claudin-low and metaplastic breast cancer subtypes. Proc Natl Acad Sci USA 2010;107(35):15449–54.; Lamouille S., Xu J., Derynck R. Molecular mechanisms of epithelial – mesenchymal transition. Nat Rev Mol Cell Biol 2014;15(3):178–96.; Platten M., Wick W., Weller M. Malignant glioma biology: role for TGF-beta in growth, motility, angiogenesis, and immune escape. Microsc Res Tech 2001;52(4):401–10.; Wesolowska A., Kwiatkowska A., Slomnicki L. et al. Microglia-derived TGF-beta as an important regulator of glioblastoma invasion – an inhibition of TGFbeta- dependent effects by shRNA against human TGF-beta type II receptor. Oncogene 2008;27(7):918–30.; Muñoz-Sanjuán I., Brivanlou A. H. Neural induction, the default model and embryonic stem cells. Nat Rev Neurosci 2002;3(4):271–80.; Ikushima H., Todo T., Ino Y. et al. Autocrine TGF-beta signaling maintains tumorigenicity of glioma-initiating cells through Sry-related HMG-box factors. Cell Stem Cell 2009;5(5):504–14.; Peñuelas S., Anido J., Prieto-Saґnchez R. M. et al. TGF-beta increases glioma-initiating cell self-renewal through the induction of LIF in human glioblastoma. Cancer Cell 2009;15(4):315–27.; Huang R. Y., Guilford P., Thiery J. P. Early events in cell adhesion and polarity during epithelial-mesenchymal transition. J Cell Sci 2012;125(Pt 19):4417–22.; Yilmaz M., Christofori G. EMT, the cytoskeleton, and cancer cell invasion. Cancer Metastasis Rev 2009;28(1–2):15–33.; Pope W. B., Chen J. H., Dong J. et al. Relationship between gene expression and enhancement in glioblastoma multiforme: exploratory DNA microarray analysis. Radiology 2008;249(1):268–77.; Zimmerman R., Peng D. J., Lanz H. et al. PP2A inactivation is a crucial step in triggering apoptin-induced tumor-selective cell killing. Cell Death Dis 2012;3:e291.; Schonthal A. H. Role of serine/threonine protein phosphatase 2A in cancer. Cancer Lett 2001;170(1):1–13.; Zhang D., Wang J., Wang Z. et al. miR-136 modulates TGF-β1-induced proliferation arrest by targeting PPP2R2A in keratinocytes. Biomed Res Int 2015;2015:453518.; Lehembre F., Yilmaz M., Wicki A. et al. NCAM-induced focal adhesion assembly: a functional switch upon loss of E-cadherin. EMBO J 2008;27(19):2603–15.; Nistico P., Bissell M. J., Radisky D. C. Epithelial-mesenchymal transition: general principles and pathological relevance with special emphasis on the role of matrix metalloproteinases. Cold Spring Harb Perspect Biol 2012;4(2):a011908.; He M., Cheng Y., Li W. et al. Vascular endothelial growth factor C promotes cervical cancer metastasis via up-regulation and activation of RhoA/ROCK-2/moesin cascade. BMC Cancer 2010;10:170.; Zhang P., Lu Y., Liu X. Y., Zhou Y. H. Knockdown of Rho-associated protein kinase 1 suppresses proliferation and invasion of glioma cells. Tumour Biol 2015;36(1):421–8.; Zhang B., Shen S., Liao Z. et al. Targeting fibronectins of glioma extracellular matrix by CLT1 peptide-conjugated nanoparticles. Biomaterials 2014;35(13):4088–98.; Galanis E., Jaeckle K. A., Maurer M. J. et al. Phase II trial of vorinostat in recurrent glioblastoma multiforme: a north central cancer treatment group study. J Clin Oncol 2009;27(12):2052–8.; Alvarez A. A., Field M., Bushnev S. et al. The effect of histone deacetylase inhibitors on glioblastoma derived cells. J Mol Neurosci 2015;55(1):7–20.; Pines G., Huang P. H., Zwang Y. et al. EGFRvIV: a previously uncharacterized oncogenic mutant reveals a kinase autoinhibitory mechanism. Oncogene 2010;29(43):5850–60.; Aitken A. 14-3-3 proteins: a historic overview. Semin Cancer Biol 2006;16(3):162–72.; Liang S., Shen G., Liu Q. et al. Isoformspecific expression and characterization of 14-3-3 proteins in human glioma tissues discovered by stable isotope labeling with amino acids in cell culture-based proteomic analysis. Proteomics Clin Appl 2009;3(6):743–53.; Cao L., Cao W., Zhang W. et al. Identification of 14-3-3 protein isoforms in human astrocytoma by immunohistochemistry. Neurosci Lett 2008;432(2): 94–9.; Yang X., Cao W., Lin H. et al. Isoformspecific expression of 14-3-3 proteins in human astrocytoma. J Neurol Sci 2009; 276(1–2):54–9.; Gong F., Wang G., Ye J. et al. 14-3-3 beta regulates the proliferation of glioma cells through the GSK3 beta/beta-catenin signaling pathway. Oncol Rep 2013;30(6):2976–82.; Salama I., Malone P. S., Mihaimeed F., Jones J. L. A review of the S100 proteins in cancer. Eur J Surg Oncol 2008;34(4): 357–64.; Du M., Wang G., Ismail T. M. et al. S100P dissociates myosin IIA filaments and focal adhesion sites to reduce cell adhesion and enhance cell migration. J Biol Chem 2012;287(19): 15330–44.; https://umo.abvpress.ru/jour/article/view/62
    • الرقم المعرف:
      10.17650/2313-805X.2016.3.2.50-59
    • الدخول الالكتروني :
      https://umo.abvpress.ru/jour/article/view/62
      https://doi.org/10.17650/2313-805X.2016.3.2.50-59
    • Rights:
      Authors who publish with this journal agree to the following terms:Authors retain copyright and grant the journal right of first publication with the work simultaneously licensed under a Creative Commons Attribution License that allows others to share the work with an acknowledgement of the work's authorship and initial publication in this journal.Authors are able to enter into separate, additional contractual arrangements for the non-exclusive distribution of the journal's published version of the work (e.g., post it to an institutional repository or publish it in a book), with an acknowledgement of its initial publication in this journal.Authors are permitted and encouraged to post their work online (e.g., in institutional repositories or on their website) prior to and during the submission process, as it can lead to productive exchanges, as well as earlier and greater citation of published work (See The Effect of Open Access). ; Авторы, публикующие статьи в данном журнале, соглашаются на следующее:Авторы сохраняют за собой автороские права и предоставляют журналу право первой публикации работы, которая по истечении 6 месяцев после публикации автоматически лицензируется на условиях Creative Commons Attribution License, которая позволяет другим распространять данную работу с обязательным сохранением ссылок на авторов оригинальной работы и оригинальную публикацию в этом журнале.Авторы имеют право размещать их работу в сети Интернет (например в институтском хранилище или персональном сайте) до и во время процесса рассмотрения ее данным журналом, так как это может привести к продуктивному обсуждению и большему количеству ссылок на данную работу (См. The Effect of Open Access).
    • الرقم المعرف:
      edsbas.427B9D82