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Emerging targets for glioblastoma stem cell therapy

The Journal of Biomedical Research 2016年第1期30卷 19-31页

作者： Ahmad R.Safa Mohammad Reza Saadatzadeh Aaron A.Cohen-Gadol Karen E.Pollok khadijeh bijangi-vishehsaraei Indiana University Simon Cancer Center IU School of Medicine and Goodman Campbell Brain and Spine Department of Pharmacology and Toxicology IU School of Medicine and Goodman Campbell Brain and Spine Department of Neurosurgery IU School of Medicine and Goodman Campbell Brain and Spine Herman B.Wells Center for Pediatric Research Indiana University School of MedicineIndianapolisIN 46202USA.

Glioblastoma multiforme（GBM）,designated as World Health Organization（WHO）grade IV astrocytoma,is a lethal and therapy-resistant brain cancer comprised of several tumor cell subpopulations,including GBM stem cells（GSCs）which are believed to contribute to tumor recurrence following initial response to *** evidence demonstrates that GBM tumors are initiated from *** development and use of novel therapies including small molecule inhibitors of specific proteins in signaling pathways that regulate sternness,proliferation and migration of GSCs,immunotherapy,and non-coding microRNAs may provide better means of treating *** and characterization of GSC-specific signaling pathways would be necessary to identify specific therapeutic targets which may lead to the development of more efficient therapies selectively targeting *** signaling pathways including mTOR,AKT,maternal embryonic leucine zipper kinase（MELK）,NOTCH1 and Wnt/β-catenin as well as expression of cancer stem cell markers CD133,CD44,Oct4,Sox2,Nanog,and ALDHlA1 maintain GSC ***,the data published in the Cancer Genome Atlas（TCGA）specifically demonstrated the activated PI3K/AKT/mTOR pathway in GBM *** such pathways may help to understand GSC biology and lead to the development of potential therapeutic interventions to render them more sensitive to chemotherapy and radiation ***,recent demonstration of dedifferentiation of GBM cell lines into CSC-like cells prove that any successful therapeutic agent or combination of drugs for GBM therapy must eliminate not only GSCs,but the differentiated GBM cells and the entire bulk of tumor cells.

关键词： glioblastoma multiforme stem cells dedifferentiation CD133 CD44 ALDHlAl SOX2

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Glioblastoma stem cells(GSCs)epigenetic plasticity and interconversion between differentiated non-GSCs and GSCs

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Genes & Diseases 2015年第2期2卷 152-163页

作者： Ahmad R.Safa Mohammad Reza Saadatzadeh Aaron A.Cohen-Gadol Karen E.Pollok khadijeh bijangi-vishehsaraei Indiana University Simon Cancer Center Indiana University School of MedicineIndianapolisIN 46202USA Department of Pharmacology and Toxicology Indiana University School of MedicineIndianapolisIN 46202USA Department of Neurosurgery IU School of Medicine and Goodman Campbell Brain and SpineIndiana University School of MedicineIndianapolisIN 46202USA Herman B.Wells Center for Pediatric Research Indiana University School of MedicineIndianapolisIN 46202USA Otolaryngology-Head and Neck Surgery Indiana University School of MedicineIndianapolisIN 46202USA

Cancer stem cells(CSCs)or cancer initiating cells(CICs)maintain self-renewal and multilineage differentiation properties of various tumors,as well as the cellular heterogeneity consisting of several subpopulations within *** display the malignant phenotype,self-renewal ability,altered genomic stability,specific epigenetic signature,and most of the time can be phenotyped by cell surface markers(e.g.,CD133,CD24,and CD44).Numerous studies support the concept that non-stem cancer cells(non-CSCs)are sensitive to cancer therapy while CSCs are relatively resistant to *** glioblastoma stem cells(GSCs),there is clonal heterogeneity at the genetic level with distinct tumorigenic potential,and defined GSC marker expression resulting from clonal evolution which is likely to influence disease progression and response to *** level of complexity in glioblastoma multiforme(GBM)tumors is the dynamic equilibrium between GSCs and differentiated non-GSCs,and the potential for non-GSCs to revert(dedifferentiate)to GSCs due to epigenetic alteration which confers phenotypic plasticity to the tumor cell ***,exposure of the differentiated GBM cells to therapeutic doses of temozolomide(TMZ)or ionizing radiation(IR)increases the GSC pool both in vitro and in *** review describes various subtypes of GBM,discusses the evolution of CSC models and epigenetic plasticity,as well as interconversion between GSCs and differentiated non-GSCs,and offers strategies to potentially eliminate GSCs.

关键词： Cancer stem cells Epigenetic GBM plasticity Glioblastoma Stemness Dedifferentiation GBM stem cells

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Human GM3 Synthase Attenuates Taxol-Triggered Apoptosis Associated with Downregulation of Caspase-3 in Ovarian Cancer Cells

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Journal of Cancer Therapy 2012年第5期3卷 504-510页

作者： Su Huang khadijeh bijangi-vishehsaraei Mohammad Reza Saadatzadeh Ahmad R. Safa Department of Medicine Division of Hematology/Oncology Indiana University School of Medicine Indianapolis USA. Department of Pharmacology and Toxicology Indiana University Simon Cancer Center Indianapolis USA

Background: Taxol (paclitaxel) inhibits proliferation and induces apoptosis in a variety of cancer cells, but it also upregulates cytoprotective proteins and/or pathways that compromise its therapeutic efficacy. Materials and Method: The roles of GM3 synthase (α2,3-sialyltransferase, ST3Gal V), in attenuating Taxol-induced apoptosis and triggering drug resistance were determined by cloning and overexpressing this enzyme in SKOV3 human ovarian cancer cell line, treating SKOV3 and the transfectants (SKOV3/GS) with Taxol and determining apoptosis, cell survival, clonogenic ability, and caspase-3 activation. Results: In this report, we demonstrated that Taxol treatment resulted in apoptosis which was associated with caspase-3 activation. Taxol treatment upregulated the expression of human GM3 synthase, an enzyme that transfers a sialic acid to lactosylceramide. Moreover, we cloned the full-length GM3 synthase gene and showed for the first time that forced expression of GM3 synthase attenuated Taxol-induced apoptosis and increased resistance to Taxol in SKOV3 cells. Conclusions: GM3 synthase overexpression inhibited Taxol-triggered caspase-3 activation, revealing that upregulation of GM3 synthase prevents apoptosis and hence reduces the efficacy of Taxol therapy.

关键词： Ovarian Cancer Taxol GM3 Synthase Apoptosis Caspase-8 Drug Resistance

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