The NFκB pathway: a therapeutic target in glioblastoma

نویسندگان

  • Lorena Nogueira
  • Patricia Ruiz-Ontañon
  • Alfonso Vazquez-Barquero
  • Francisco Moris
  • Jose L. Fernandez-Luna
چکیده

Cancer initiating cells have been described to be the only cell population with tumorigenic capacity in glioblastoma multiforme, one of the most aggressive and untreatable cancers. Recent work from our group described that NFκB pathway was activated in glioblastoma initiating cells undergoing differentiation, and that blockade of this activation promoted senescence of differentiating cells. NFκB activation in cancer may be the result of either exposure to proinflammatory stimuli in the tumor microenvironment or upregulation of the signaling pathway by upstream regulators. Appropriate control of NFκB activity, which can be achieved by gene modification or pharmacological strategies, would provide a potential approach for the management of NFκB related tumors, including glioblastoma. Here, we summarize the current knowledge of the relevance of NFκB in cancer and its possible role as a target of therapeutic intervention..

برای دانلود رایگان متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

The Role of Mammalian Target of Rapamycine Signaling Pathway in Central Nervous System Cancers: A Review

Mammalian mechanistic target of rapamycine (mTOR) is a conserved serine/threonine kinase in the cellular PI3K/Akt/mTOR signaling pathway. This pathway is modified by cellular alterations such as level of energy, growth factors, stresses, as well as the increased environmental level of cancerous cytokines. In general, increase of this kinase protein function is seen in various types of cancers, ...

متن کامل

Inhibition of IKK-NFκB pathway sensitizes lung cancer cell lines to radiation

OBJECTIVE : Cancer cell radioresistance is a stumbling block in radiation therapy. The activity in the nuclear factor kappa B (NFκB) pathway correlates with anti-apoptotic mechanisms and increased radioresistance. The IKK complex plays a major role in NFκB activation upon numerous signals. In this study, we examined the interaction between ionizing radiation (IR) and different members of the IK...

متن کامل

Investigating specific expression of ADAM29, FTHL17, and HORMAD1 cancer/testis genes in glioblastoma tumors

Introduction: Glioblastoma primary brain tumor.Immunotherapy is a promising therapeutic adjuvant in fighting against this cancer.  Cancer/testis antigens (CTAs) are a group of tumor-associated antigens that are typically restricted to adult testis, but they are aberrantly expressed in several types of cancers, especially in advanced cancers with stem-like characteristics. These tumor-associate...

متن کامل

Down-regulation of IKKβ expression in glioma-infiltrating microglia/macrophages is associated with defective inflammatory/immune gene responses in glioblastoma

Glioblastoma (GBM) is an aggressive malignancy associated with profound host immunosuppression. Microglia and macrophages infiltrating GBM acquire the pro-tumorigenic, M2 phenotype and support tumor invasion, proliferation, survival, angiogenesis and block immune responses both locally and systematically. Mechanisms responsible for immunological deficits in GBM patients are poorly understood. W...

متن کامل

Effects of Trichostatin A on the Histone Deacetylases (HDACs), Intrinsic Apoptotic Pathway, p21/Waf1/Cip1, and p53 in Human Neuroblastoma, Glioblastoma, Hepatocellular Carcinoma, and Colon Cancer Cell Lines

Background:  The aberrant and altered patterns of gene expression play an important role in the biology of cancer and tumorigenesis. DNA methylation and histone deacetylation are the most studied epigenetic mechanisms. Histone deacetylase inhibitors (HDACIs) such as valproic acid (VPA) and trichostatin A (TSA) are a group of anticancer compounds for the treatment of solid and hematological canc...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

عنوان ژورنال:

دوره 2  شماره 

صفحات  -

تاریخ انتشار 2011