Molecular mechanisms of programmed cell death

McKenna, Sharon L.; McGowan, Adrian J.; Cotter, Thomas G.

doi:10.1007/bfb0102304

Cited by 9 publications

(7 citation statements)

References 165 publications

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“…Apoptosis (programmed cell death), is a process of cellular destruction that is required for the development and homeostasis of multicellular organisms (32). Apoptosis is characterized by cell shrinkage, condensation of nuclei and internucleosomal degradation of DNA.…”

Section: Introductionmentioning

confidence: 99%

Apoptotic activity of 5-fluorouracil in breast cancer cells transformed by low doses of ionizing α-particle radiation

Ponce‐Cusi

Calaf

2015

International Journal of Oncology

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Globally, breast cancer in women is the leading cause of cancer death. This fact has generated an interest to obtain insight into breast tumorigenesis and also to develop drugs to control the disease. Ras is a proto-oncogene that is activated as a response to extracellular signals. As a member of the Ras GTPase superfamily, Rho-A is an oncogenic and a critical component of signaling pathways leading to downstream gene regulation. In chemotherapy, apoptosis is the predominant mechanism by which cancer cells die. However, even when the apoptotic machinery remains intact, survival signaling may antagonize the cell death by signals. The aim of this study was to evaluate 5-fluorouracil (5-FU) in cells transformed by low doses of ionizing α-particle radiation, in breast cancer cell lines on these genes, as well as apoptotic activity. We used two cell lines from an in vitro experimental breast cancer model. The MCF-10F and Tumor2 cell lines. MCF-10F was exposed to low doses of high linear energy transfer (LET) α-particles radiation (150 keV/µm). Tumor2, is a malignant and tumorigenic cell line obtained from Alpha5 (60cGy+E/60cGy+E) injected into the nude mice. Results indicated that 5-FU decreased H-ras, Rho-A, p53, Stat1 and increased Bax gene expression in Tumor2 and decreased Rac1, Rho-A, NF-κB and increased Bax and caspase-3 protein expression in Tumor2. 5-FU decreased H-ras, Bcl-xL and NF-κB and increased Bax gene expression. 5-FU decreased Rac1, Rho-A protein expression and increased Bax and caspase-3 protein expression in MDA-MB-231. Flow cytometry indicated 21.5% of cell death in the control MCF-10F and 80% in Tumor2 cell lines. It can be concluded that 5-FU may exert apoptotic activity in breast cancer cells transformed by low doses of ionizing α-particles in vitro regulating genes of Ras family and related to apoptosis such as Bax, Bcl-xL and NF-κB expression.

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Section: Introductionmentioning

confidence: 99%

Apoptotic activity of 5-fluorouracil in breast cancer cells transformed by low doses of ionizing α-particle radiation

Ponce‐Cusi

Calaf

2015

International Journal of Oncology

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“…The initiating triggers are many and varied, and are grouped broadly as physiological or nonphysiological. These include, but are not limited to, the following: Fas ligands (Fas), tumour necrosis factor (TNF), nerve growth factor (NGF), nitric oxide (NO), lipopolysaccharide (LPS), host immune reactions, kinins and glucocorticoids (McKenna et al . 1998).…”

Section: Introductionmentioning

confidence: 99%

Apoptosis: an introduction for the endodontist

Satchell

Gutmann

Witherspoon³

2003

Int Endodontic J

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Apoptosis plays an important role in many aspects of endodontics, yet there is a paucity of information in this regard in the endodontic literature. Apoptosis is a single deletion of scattered cells by fragmentation into membrane-bound particles that are phagocytosed by other cells. It is a key process in the embryological development of the tooth, periodontal ligament and supporting oral tissue in the progression of oral disease, bone resorption, immunological response and inflammation, and in wound healing and certain pharmacological effects. The understanding of the ability of clinical materials to induce or inhibit apoptosis and the investigation of apoptosis as it relates to the pathogenesis of pulpal and periradicular pathology may eventually lead to new treatment approaches for the endodontist. The purpose of this review is to familiarize the clinical endodontist with current knowledge on apoptosis as it relates to the pulp and periradicular tissues.

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“…[1][2][3] Ligation of the receptors for Fas/TNF can lead directly to activation of caspases, which can act as effectors of cell death by catalyzing structural changes associated with apoptosis, including cytoskeletal reorganization and DNA fragmentation. Survival factors mediate signals through several kinases, such as phosphoinositol 3 kinase and AKT, ultimately leading to transcriptional events or to regulation of Bcl-2 family proteins.…”

Section: Introductionmentioning

confidence: 99%

Erythrocyte survival is promoted by plasma and suppressed by a Bak-derived BH3 peptide that interacts with membrane-associated Bcl-XL

Walsh

Lutz

Cotter

et al. 2002

Blood

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Erythrocytes have a defined lifespan in vivo, and the signals that maintain their survival in circulation or trigger their death are unknown. Here, we investigated the control of erythrocyte survival and death in an in vitro culture system where erythrocytes survived for 10 days in serumfree medium in the presence or absence of bovine serum. Death of the cells in culture was correlated with increased exposure of phosphatidylserine and increased levels of intracellular calcium. Cell death could be suppressed by supplementing the medium with human plasma or serum, resulting in a doubling of the lifespan to 20 days. Freshly isolated erythrocytes and cultured erythrocytes were both found to express Bcl-X L and, to a lesser extent, Bak in membrane protein extracts. Treatment of the cells with a Bak-derived BH3 peptide fused to the internalization sequence of the antennapedia protein, which has previously been shown to enter cells by diffusion and antagonize Bcl-X L , resulted in substantial cell death in erythrocyte cultures. BH3-induced death was accompanied by an immediate increase in accumulation of intracellular calcium and could be suppressed by plasma, but not by the caspase inhibitor zVAD. A BH3 peptide mutated at amino acid 78 of full-length Bak required for heterodimerization with Bcl-X L had no effect on cell viability or calcium levels. We conclude that the BH3 peptide accelerates erythrocyte death through antagonization of Bcl-X L . The data suggest that erythrocyte survival is promoted by survival factors in plasma and by membrane- IntroductionCell death and survival in hematopoietic cells is regulated by signals from cell-surface receptors that either promote apoptosis, such as Fas and tumor necrosis factor (TNF), or repress cell death, such as receptors for cytokines and survival factors such as erythropoietin (EPO), interleukin 3, and insulinlike growth factor I (IGF-I). [1][2][3] Ligation of the receptors for Fas/TNF can lead directly to activation of caspases, which can act as effectors of cell death by catalyzing structural changes associated with apoptosis, including cytoskeletal reorganization and DNA fragmentation. Survival factors mediate signals through several kinases, such as phosphoinositol 3 kinase and AKT, ultimately leading to transcriptional events or to regulation of Bcl-2 family proteins. 4 The Bcl-2 family acts as central regulators of cell death in many cells [5][6][7] and is divided into 2 main groups consisting of suppressors of apoptosis, including Bcl-2, Bcl-X L , Bcl-w, and Mcl-1, and potent apoptosis promoters, including Bax, Bak, Bad, and Bid. Bcl-2 and Bcl-X L survival activity can be antagonized by heterodimerization with proteins containing a BH3 domain, which is the essential domain for the binding and proapoptotic activity of Bak, Bax, Bik, and Bid. 8 Bcl-2 and Bcl-X L are expressed in outer mitochondrial membranes where antagonization of their function is associated with rupture of the membrane, release of the proapoptotic factors cytochrome c, and activation of caspas...

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Molecular mechanisms of programmed cell death

Cited by 9 publications

References 165 publications

Apoptotic activity of 5-fluorouracil in breast cancer cells transformed by low doses of ionizing α-particle radiation

Apoptotic activity of 5-fluorouracil in breast cancer cells transformed by low doses of ionizing α-particle radiation

Apoptosis: an introduction for the endodontist

Erythrocyte survival is promoted by plasma and suppressed by a Bak-derived BH3 peptide that interacts with membrane-associated Bcl-XL

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