Apoptin-induced cell death is modulated by Bcl-2 family members and is Apaf-1 dependent

Burek, Małgorzata; Maddika, Subbareddy; Burek, Christof; Daniel, Peter T.; Schulze‐Osthoff, Klaus; Łos, Marek

doi:10.1038/sj.onc.1209258

Cited by 71 publications

(78 citation statements)

References 56 publications

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“…Une des caractéristiques remarquables de cette protéine est sa capacité à induire directement l'apoptose et ce spécifiquement dans les cellules tumorales, les cellules primaires et non transformées étant résis-tantes [31]. Ce phénomène est dépendant de Bcl-2 et des caspases, et fait intervenir Apaf1 (apoptotic peptidase activating factor 1) et l'apoptosome dans l'induction de la mort induite par la mitochondrie [32]. L'insertion de cette protéine apoptine dans un virus comme le VSV pourrait conférer des propriétés oncolytiques additionnelles très intéressantes.…”

Section: Promouvoir L'implication Du Système Immunitaireunclassified

Le virus de la stomatite vésiculaire dans la lutte contre le cancer

2013

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Section: Promouvoir L'implication Du Système Immunitaireunclassified

Le virus de la stomatite vésiculaire dans la lutte contre le cancer

2013

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“…Several models have been proposed to elucidate risk factors, such as smoking and alcoholic beverages. Genetic and epidemiological markers are involved in the generation and progress of OSCC [26,94]. According to the multi-step carcinogenesis concept, OSCC develops in a series of more or less defined intermediate stages through the accumulation of molecular changes and progression from a pre-cancerous leukoplakia to pre-invasive (erythroplakia) and finally to the invasive cancer disease with lymphonodal outspread and severe local destruction [122,137].…”

Section: Oral Squamous Cell Carcinomamentioning

confidence: 99%

Cancer stem cells as targets for cancer therapy: selected cancers as examples

Hombach‐Klonisch

Paranjothy

Wiecheć

et al. 2008

Arch. Immunol. Ther. Exp.

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It is becoming increasingly evident that cancer constitutes a group of diseases involving altered stem-cell maturation/differentiation and the disturbance of regenerative processes. The observed malignant transformation is merely a symptom of normal differentiation processes gone astray rather than the primary event. This review focuses on the role of cancer stem cells (CSCs) in three common but also relatively under-investigated cancers: head and neck, ovarian, and testicular cancer. For didactic purpose, the physiology of stem cells is first introduced using hematopoietic and mesenchymal stem cells as examples. This is followed by a discussion of the (possible) role of CSCs in head and neck, ovarian, and testicular cancer. Aside from basic information about the pathophysiology of these cancers, current research results focused on the discovery of molecular markers specific to these cancers are also discussed. The last part of the review is largely dedicated to signaling pathways active within various normal and CSC types (e.g. Nanog, Nestin, Notch1, Notch2, Oct3 and 4, Wnt). Different elements of these pathways are also discussed in the context

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“…(c) Induction of apoptosis by the different apoptin mutants. The percentage of apoptosis was assessed in PC-3 cells by flow cytometric detection of hypodiploid DNA (left panel) and in MCF-7 cells by the MTT assay (right panel) 24 h post-transfection essentially as described previously (Maddika et al, 2005;Burek et al, 2006).…”

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confidence: 99%

Interaction with PI3-kinase contributes to the cytotoxic activity of Apoptin

et al. 2007

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Apoptin, a small protein from the chicken anemia virus, has attracted attention because of its specificity in killing tumor cells. Localization of apoptin in the nucleus of tumor cells has been shown to be vital for proapoptotic activity, however, targeted expression of apoptin in the nucleus of normal cells does not harm the cells, indicating that nuclear localization of apoptin is insufficient for its cytotoxicity. Here, we demonstrate for the first time that apoptin interacts with the SH3 domain of p85, the regulatory subunit of phosphoinositide 3-kinase (PI3-K), through its proline-rich region. Apoptin derivatives devoid of this proline-rich region do not interact with p85, are unable to activate PI3-K, and show impaired apoptosis induction. Moreover, apoptin mutants containing the proline-rich domain are sufficient to elevate PI3-K activity and to induce apoptosis in cancer cells. Downregulation of p85 leads to nuclear exclusion of apoptin and impairs cell death induction, indicating that interaction with the p85 PI3-K subunit essentially contributes to the cytotoxic activity of apoptin.

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Apoptin-induced cell death is modulated by Bcl-2 family members and is Apaf-1 dependent

Cited by 71 publications

References 56 publications

Le virus de la stomatite vésiculaire dans la lutte contre le cancer

Le virus de la stomatite vésiculaire dans la lutte contre le cancer

Cancer stem cells as targets for cancer therapy: selected cancers as examples

Interaction with PI3-kinase contributes to the cytotoxic activity of Apoptin

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