Special Issue "Cell Death and Cancer"
QuicklinksA special issue of Cancers (ISSN 2072-6694).
Deadline for manuscript submissions: closed (30 December 2010)
Special Issue Editor
Guest Editor
Prof. Dr. Afshin Samali
Head of Biochemistry, School of Natural Sciences, National University of Ireland - Galway, University Road, Galway, Ireland
Website: http://www.nuigalway.ie/biochemistry/staff/samali/index.html
E-Mail:
Phone: +353 91 492440
Fax: +353 91 494596
Interests: apoptosis; cell death; autophagy; TRAIL; heat shock proteins; Endoplasmic Reticulum stress; hypoxia
Published Papers
Special Issue Information
Dear Colleagues,
Cell death is involved in a variety of biological processes including morphogenesis, maintaining tissue homeostasis and elimination of harmful cells. Deregulation of proliferation, together with a reduction in cell death, is both necessary and sufficient for tumor development, progression, and resistance to therapy. The mechanisms of cell death and cell survival are complex and involve not only apoptosis and necrosis, but also their cross-talk with other programmed intracellular processes such as autophagy. In addition, the tumor microenvironment has a great impact on cell death, cell signaling, tumor metabolism, cell survival, and therapeutic responsiveness. The central focus of the special issue on “Cell Death and Cancer” is cell death regulation and how to exploit it for therapeutic gain. The main topics will include, but are not limited to, the role of cell death (e.g., apoptosis and necrosis) and cell survival pathways (e.g., autophagy) in tumorigenesis; targeting autophagy and cell death pathways for tumor eradication; death receptor and mitochondria-mediated apoptosis; stress-activated and survival-related protein kinases (e.g., p38, JNK, AKT, etc.) and their role in cell death; novel strategies to target anti-apoptotic proteins (SMAC mimetics, BH3 mimetics etc.).
Thank you for your collaboration.
Prof. Dr. Afshin Samali
Guest Editor
Submission
Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. Papers will be published continuously (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.
Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are refereed through a peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cancers is an international peer-reviewed Open Access quarterly journal published by MDPI.
Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 500 CHF (Swiss Francs). English correction and/or formatting fees of 250 CHF (Swiss Francs) will be charged in certain cases for those articles accepted for publication that require extensive additional formatting and/or English corrections.
Keywords
- apoptosis
- autophagy
- Bcl-2 family
- caspases
- cell death
- cell survival
- death receptors
- mitochondria
- oncogenes
- tumor suppressor genes
Planned Papers
Title: Mechanisms and Therapeutic Implications of Cell Death Induction by Indole Compounds
Authors: Aamir Ahmad, Wael A. Sakr and K.M. Wahidur Rahman
Affiliation: Department of Pathology, Karmanos Cancer Institute, Wayne State University School of Medicine, Detroit, MI 4820, USA;
E-Mail: kmrahman@med.wayne.edu (K.M.W.R.)
Abstract: Indole compounds, obtained from cruciferous vegetables, are well-known for their anti-cancer properties. In particular, indole-3-carbinol (I3C) and its dimeric product, 3, 3' diindolylmethane (DIM), have been investigated widely for their effectiveness against a number of human cancers in vitro as well as in vivo. These compounds are effective inducers of apoptosis and the accumulating evidence documenting their ability to modulate multiple cellular signaling pathways is a testimony to their pleiotropic behavior. Here we attempt to update current understanding on the various mechanisms that are responsible for the apoptosis-inducing effects by these compounds. The significance of apoptosis-induction as a desirable attribute of anti-cancer agents such as indole compounds can not be over-stated. However, an equally intriguing property of these compounds is their ability to sensitize cancer cells to standard chemotherapeutic agents. Such chemosensitizing effects of indole compounds can potentially have major clinical implications because these non-toxic compounds can reduce the toxicity and drug-resistance associated with available chemotherapies. Combinational therapy is increasingly being realized to be better than single agent therapy and, through this review article, we aim to provide a rationale behind combination of natural compounds such as indoles with conventional therapeutics.
Type of Paper: Review
Title: Radical Decisions in Cancer: Redox Control of Cell Growth and Death
Author: Rosa M. Sainz
Affiliation: Department of Cellular and Structural Biology, Cancer Research Institute PA (IUOPA), School of Medicine. Lab 9.12, University of Oviedo, Spain; E-Mail: sainzrosa@uniovi.es
Abstract: Free radicals play a key role in many physiological decisions in cells. Since free radicals are toxic molecules for cellular components, it is known that they can cause DNA damage, contribute to DNA instability and mutation and then, favour carcinogenesis. However, nowadays it is assumed that free radicals play a further complex role in cancer. Low levels of free radicals and steady state of antioxidant enzymes are responsible of a fine tuning of redox status inside cells. A change in redox state is a way to modify the physiological status of the cell, in fact, a more reduced status is found in resting cells while a more oxidative status associated with in proliferative cells. The mechanisms by which redox status can change proliferative activity of cancer cells are related with transcriptional and posttranscriptional modifications of proteins that play a critical role in cell cycle control. Since cancer cells show higher levels of free radicals compared with their normal counterparts, it is believed that the mechanism against oxidative stress is also increased in cancer cells. In fact, the levels of some of the most important antioxidant enzymes are elevated in advanced status of some types of tumors. Cancer treatment is compromised by survival mechanisms in cancer cells and collateral damage in normal non pathological tissues. Though some resistance mechanisms have been described, but yet, they do not explain cancer treatment failure in several tumors. Given that some antitumoral treatments are based on the generation of free radicals, we will discuss in this review the possible role of antioxidant enzymes in the survival mechanism in cancer cells and then, its participation in the failure of cancer treatments.
Type of Paper: Review
Title: Nuclear Receptor Small Heterodimer Partner in Apoptosis Signaling and Liver Cancer
Author: Li Wang
Affiliation: Departments of Medicine and Oncological Sciences, Huntsman Cancer Institute, University of Utah School of Medicine, Salt Lake City, UT 84132, USA; E-Mail: l.wang@hsc.utah.edu
Abstract: Small heterodimer partner (SHP, NR0B2) is a unique orphan nuclear receptor in the nuclear receptor superfamily in that it lacks a DNA binding domain and endogenous ligands, and functions as a transcriptional repressor. We have recently shown that SHP knockout (SHP-/-) mice were prone to the development of liver tumors which was associated with hepatocyte hyperproliferation and that SHP expression was diminished in human hepatocellular carcinoma by an epigenetic mechanism. In this review we focus on our recent finding of the novel regulatory role of SHP in mitochondria function and apoptosis signaling associated with the development of liver cancer. We for the first time show that as a well characterized nuclear protein and transcription factor, SHP is able to shuttle between the nucleus and mitochondria by its interacting partner hepatocyte nuclear factor 4 alpha (HNF4α) and its synthetic agonist retinoid 6-[3-(1-adamantyl)-4-hydroxyphenyl]-2-naphthalene carboxylic acid (AHPN), the later is a known apoptosis inducer. SHP mitochondrial targeting plays a crucial role in its interacting with the antiapoptotic protein Bcl-2, inducing cytochrome c release and activating cellular apoptosis. Thus, SHP appears to be a novel component of the cell death pathway and SHP activation of hepatocyte apoptosis is critical for its inhibition of liver cancer progression.
Keywords: nuclear receptor; mitochondria; apoptosis; liver cancer
Last update: 12 May 2011