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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Shoshan-barmatz, Varda Arif, Tasleem Krelin, Yakov |
| Description | Author Affiliation: Arif T ( Department of Life Sciences and the National Institute for Biotechnology in the Negev, Ben-Gurion University of the Negev, Beer-Sheva 84105, Israel.); Krelin Y ( Department of Life Sciences and the National Institute for Biotechnology in the Negev, Ben-Gurion University of the Negev, Beer-Sheva 84105, Israel.); Shoshan-Barmatz V ( Department of Life Sciences and the National Institute for Biotechnology in the Negev, Ben-Gurion University of the Negev, Beer-Sheva 84105, Israel. Electronic address: vardasb@bgu.ac.il.) |
| Abstract | Proteins initially identified as essential for apoptosis also mediate a wide range of non-apoptotic functions that include cell cycle progression, differentiation and metabolism. As this phenomenon was mostly reported with non-cancer cells, we considered non-conventional roles for the apoptotic machinery in the cancer setting. We found that treating glioblastoma (GBM) tumors with siRNA against VDAC1, a mitochondrial protein found at the crossroads of metabolic and survival pathways and involved in apoptosis, inhibited tumor growth while leading to differentiation of tumor cells into neuronal-like cells, as reflected in the expression of specific markers. Although VDAC1 depletion did not induce apoptosis, the expression levels of several pro-apoptotic regulatory proteins were changed. Specifically, VDAC1 deletion led to up-regulation of caspases, p53, cytochrome c , and down-regulation of SMAC/Diablo, AIF and TSPO. The down-regulated group was highly expressed in U-87MG xenografts, as well as in GBMs from human patients. We also showed that the rewired cancer-cell metabolism resulting from VDAC1 depletion reinforced cell growth arrest and differentiation via alterations in the transcription factors p53, c-Myc, HIF-1α and NF-κB. The decrease in c-Myc, HIF-1α and NF-κB levels was in accord with reduced cell proliferation, whereas increased p53 expression promoted differentiation. Thus, upon metabolic re-programing induced by VDAC1 depletion, the levels of pro-apoptotic proteins associated with cell growth decreased, while those connected to cell differentiation increased, converting GBM cells into astrocyte- and neuron-like cells. The results reveal that in tumors, pro-apoptotic proteins can perform non-apoptotic functions, acting as regulators of cell growth and differentiation, making these molecules potential new targets for cancer therapy. This article is part of a Special Issue entitled ‘EBEC 2016: 19th European Bioenergetics Conference, Riva del Garda, Italy, July 2–6, 2016’, edited by Prof. Paolo Bernardi. |
| ISSN | 00063002 |
| Journal | Biochimica et Biophysica Acta (BBA) - Reviews on Cancer |
| Issue Number | 8 |
| Volume Number | 1857 |
| Language | English |
| Publisher | Elsevier |
| Publisher Date | 2016-08-01 |
| Publisher Place | Netherlands |
| Access Restriction | Open |
| Subject Keyword | Brain Neoplasms Therapy Gene Expression Regulation, Neoplastic Glioblastoma Mitochondria Metabolism RNA, Small Interfering Genetics Voltage-Dependent Anion Channel 1 Animals Apoptosis Apoptosis Inducing Factor Pathology Caspases Cell Differentiation Cell Line, Tumor Cell Proliferation Cytochromes c Hypoxia-Inducible Factor 1, Alpha Subunit Intracellular Signaling Peptides And Proteins Mice Mice, Nude Mitochondrial Proteins NF-kappa B Neurons Proto-Oncogene Proteins C-myc Receptors, GABA Signal Transduction Tumor Suppressor Protein P53 Antagonists & Inhibitors Xenograft Model Antitumor Assays Research Support, Non-U.S. Gov't Biochemistry |
| Content Type | Text |
| Resource Type | Article |
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