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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Weisthal, Shira Ben-hail, Danya Keinan, Nurit Shoshan-barmatz, Varda Arif, Tasleem |
| Description | Author Affiliation: Weisthal S ( Department of Life Sciences and the National Institute for Biotechnology in the Negev, Ben-Gurion University of the Negev, Beer-Sheva 84105, Israel.); Keinan N ( Department of Life Sciences and the National Institute for Biotechnology in the Negev, Ben-Gurion University of the Negev, Beer-Sheva 84105, Israel.); Ben-Hail D ( Department of Life Sciences and the National Institute for Biotechnology in the Negev, Ben-Gurion University of the Negev, Beer-Sheva 84105, Israel.); 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.); 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 | VDAC1, an outer mitochondrial membrane (OMM) protein, is crucial for regulating mitochondrial metabolic and energetic functions and acts as a convergence point for various cell survival and death signals. VDAC1 is also a key player in apoptosis, involved in cytochrome c (Cyto c ) release and interactions with anti-apoptotic proteins. Recently, we demonstrated that various pro-apoptotic agents induce VDAC1 oligomerization and proposed that a channel formed by VDAC1 oligomers mediates cytochrome c release. As VDAC1 transports Ca $^{2$ + across the OMM and because Ca $^{2$ + has been implicated in apoptosis induction, we addressed the relationship between cytosolic Ca $^{2$ + levels ([Ca $^{2}$ $^{+}$ ]i), VDAC1 oligomerization and apoptosis induction. We demonstrate that different apoptosis inducers elevate cytosolic Ca $^{2$ + and induce VDAC1 over-expression. Direct elevation of [Ca $^{2$ + ]i by the Ca $^{2$ + -mobilizing agents A23187, ionomycin and thapsigargin also resulted in VDAC1 over-expression, VDAC1 oligomerization and apoptosis. In contrast, decreasing [Ca $^{2$ + ]i using the cell-permeable Ca $^{2$ + -chelating reagent BAPTA-AM inhibited VDAC1 over-expression, VDAC1 oligomerization and apoptosis. Correlation between the increase in VDAC1 levels and oligomerization, [Ca $^{2$ + ]i levels and apoptosis induction, as induced by H $_{2}$ O $_{2}$ or As $_{2}$ O $_{3}$ , was also obtained. On the other hand, cells transfected to overexpress VDAC1 presented Ca $^{2$ + -independent VDAC1 oligomerization, cytochrome c release and apoptosis, suggesting that [Ca $^{2$ + ]i elevation is not a pre-requisite for apoptosis induction when VDAC1 is over-expressed. The results suggest that Ca $^{2$ + promotes VDAC1 over-expression by an as yet unknown signaling pathway, leading to VDAC1 oligomerization, ultimately resulting in apoptosis. These findings provide a new insight into the mechanism of action of existing anti-cancer drugs involving induction of VDAC1 over-expression as a mechanism for inducing apoptosis. This article is part of a Special Issue entitled: Calcium Signaling in Health and Disease. Guest Editors: Geert Bultynck, Jacques Haiech, Claus W. Heizmann, Joachim Krebs, and Marc Moreau |
| ISSN | 00063002 |
| Journal | Biochimica et Biophysica Acta (BBA) - Reviews on Cancer |
| Issue Number | 10 |
| Volume Number | 1843 |
| Language | English |
| Publisher | Elsevier |
| Publisher Date | 2014-10-01 |
| Publisher Place | Netherlands |
| Access Restriction | Open |
| Subject Keyword | Calcium Signaling Calcium Metabolism Gene Expression Regulation Mitochondria Mitochondrial Membranes Voltage-Dependent Anion Channel 1 Genetics Calcimycin Pharmacology Calcium Ionophores Cell Death Drug Effects Cell Line, Tumor Cell Survival Chelating Agents Cytochromes c Secretion Egtazic Acid Analogs & Derivatives Hydrogen Peroxide Ionomycin Protein Multimerization Thapsigargin Research Support, Non-U.S. Gov't Biochemistry |
| Content Type | Text |
| Resource Type | Article |
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