Survivin inhibition by an interacting recombinant peptide, derived from the human ferritin heavy chain, impedes tumor cell growth

Weiß, Astrid; Brill, Boris; Borghouts, Corina; Delis, Natalia; Mack, Laura; Groner, Bernd

doi:10.1007/s00432-012-1195-1

Cited by 17 publications

(19 citation statements)

References 56 publications

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“…Human hepatoma cells, when transfected with survivin-specific siRNA, showed an increase in response to radiotherapy with LET carbon ions. Silencing the wild-type survivin led to an increase in apoptosis, decrease in clonogenic capacity of the cancer cells and increased the caspase-3 levels in the cancer cells [72,73]. Another study supporting this finding is the use of siRNA against survivin to enhance the effects of curcumin for hepatocellular carcinoma (HCC) cells.…”

Section: Gene Silencing Methodsmentioning

confidence: 84%

Clinical aspects for survivin: a crucial molecule for targeting drug-resistant cancers

Singh

Krishnakumar

Kanwar

et al. 2015

Drug Discovery Today

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Section: Gene Silencing Methodsmentioning

confidence: 84%

Clinical aspects for survivin: a crucial molecule for targeting drug-resistant cancers

Singh

Krishnakumar

Kanwar

et al. 2015

Drug Discovery Today

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“…Further studies are needed to confirm the physiological relevance of the data. A peptide corresponding to amino acids 19 to 125 of the human FtH has been shown to interact with surviving, an anti-apoptotic protein strongly expressed in different types of cancer cells (Weiss et al 2012). The peptide, expressed as a fusion protein with a variant of the human thioredoxin protein, was able to target the anti-apoptotic function of survivin and cause tumor cell death.…”

Section: Mammalian Cytosolic Ferritin Not Only Ironmentioning

confidence: 99%

Biology of ferritin in mammals: an update on iron storage, oxidative damage and neurodegeneration

2014

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Iron is an abundant transition metal that is essential for life, being associated to many enzyme and oxygen carrier proteins involved in a variety of fundamental cellular processes. At the same time the metal is potentially toxic due to its capacity to engage in the catalytic production of noxious reactive oxygen species. The control of iron availability in the cells is largely dependent on ferritins, ubiquitous proteins with storage and detoxification capacity. In mammals, cytosolic ferritins are composed of two types of subunits, the H and the L chain, assembled to form a 24-mer spherical cage. Ferritin is present also in mitochondria, in the form of a complex with 24 identical chains. Even though the proteins have been known for a long time, their study is a very active and interesting field yet. In this review we will focus our attention to mammalian cytosolic and mitochondrial ferritins, describing the most recent advancement regarding their storage and antioxidant function, the effects of their genetic mutations in human pathology, and also the possible involvement in non-iron related activities. We will also discuss recent evidence connecting ferritins and the toxicity of iron in a set of neurodegenerative disorder characterized by focal cerebral siderosis. IntroductionThe adaptation of life to an oxic environment required the development of mechanisms to deal with the transformation of the water soluble ferrous ion (Fe 2+ ) to the insoluble ferric ion (Fe 3+ ) and with the concomitant generation of dangerous reactive oxygen species (ROS). The ferritin molecules represent an important and ancient mean developed by organisms in the three domains of life to safely handle the necessary, yet potentially toxic metal. Their ability to detoxify and store the metal through safe oxidation processes protects the cells from undue iron-dependent redox chemistry, while a controlled release of the metal guarantees its availability for different and essential enzymatic reactions. Storage and detoxification of iron represent the main functions of these molecules, and much work has been done to understand the chemical and molecular details of this

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“…Despite the difficulties, numerous ways concerning survivin inhibition have been utilized and depend mostly on indirect mechanisms, e.g., by interference with the expression of the survivin gene, its mRNA processing, the intracellular localization and the binding partners, or by affecting stability of survivin protein or by provoking survivin-specific immune responses [34] . Research is continuing in order to deploy drugs which cooperate with survivin and restrain its operation [34,35] .…”

Section: Approaches For Targeting Survivin Isoformsmentioning

confidence: 99%

Association of survivin splice variants with prognosis and treatment of breast cancer

Pavlidou

Kroupis

Dimas

2014

WJCO

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The purpose of this study was the overview of current knowledge regarding the use of survivin and its isoforms in prognosis and treatment of breast cancer. An advanced search of Medline was performed using the following search strategy: "(survivin isoforms) OR (survivin transcript variants) AND (breast cancer) AND (neoplasm OR tumor OR cancer OR carcinoma)". Relevant studies were retrieved and processed thoroughly in order to analyze the related data. Besides wild-type survivin full-length transcript, another six splice variants have been identified. Overexpression of survivin and its isoforms leads to shorter overall and disease-free survival; the transcript variants are correlated with apoptosis and could assist prognosis prediction. It has been proved through numerous studies that inhibiting survivin isoforms might become a promising target of drug therapy of carcinomas. Use of small molecule YM155 could offer new therapy for triple negative breast cancer patients, while, chemotherapy with 5-fluorouracil + epirubicin + cyclophosphamide and Tax-Epi could be guided by survivin splice variants measurements. Survivin transcript variants could become prognostic biomarkers and could provide information about clinical management of patients suffering from breast cancer.© 2014 Baishideng Publishing Group Inc. All rights reserved.Key words: Survivin gene; Isoforms; Therapy; Prognosis; Breast cancer Core tip: Besides wild type survivin full length transcript, another six splice variants have been identified. Overexpression of survivin and its isoforms leads to shorter overall and disease-free survival; the transcript variants are positively correlated with apoptosis and could assist prognosis prediction. It has been proved through numerous studies that inhibiting survivin isoforms might become a promising target of drug therapy of carcinomas. Use of small molecule YM155 could offer new therapy for triple negative breast cancer patients while, chemotherapy with 5-fluorouracil + epirubicin + cyclophosphamide and Tax-Epi could be guided by survivin splice variants measurements. Survivin transcript variants could become prognostic biomarkers and could provide information about clinical management of patients suffering from breast cancer.Pavlidou A, Kroupis C, Dimas K. Association of survivin splice variants with prognosis and treatment of breast cancer. World J

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Survivin inhibition by an interacting recombinant peptide, derived from the human ferritin heavy chain, impedes tumor cell growth

Abstract: rSip provides a lead structure for the development of drugs targeting the tumor cell "addiction protein" survivin.

Cited by 17 publications

References 56 publications

Clinical aspects for survivin: a crucial molecule for targeting drug-resistant cancers

Clinical aspects for survivin: a crucial molecule for targeting drug-resistant cancers

Biology of ferritin in mammals: an update on iron storage, oxidative damage and neurodegeneration

Association of survivin splice variants with prognosis and treatment of breast cancer

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