Survivin in skin pathologies

Bongiovanni, Laura; Müller, Eliane J.; Salda, Leonardo Della

doi:10.1111/j.1600-0625.2011.01273.x

Cited by 25 publications

(39 citation statements)

References 149 publications

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“…In the present study, highest levels of expression of nuclear p53 were significantly associated with a shorter post surgical OS, and appeared to be related to the development of metastasis, confirming the importance of p53 as a negative prognostic marker in canine OSA, in accordance to previous published data regarding canine OSA, suggesting that, similarly to human OSA [68,69], alterations in p53 functions are associated with highly aggressive tumour behaviour [70,71]. Deregulation of the p53-survivin subsystem has been proposed to play an important role in several tumour types [72], since, WTp53 is able to repress survivin expression at both the mRNA and protein level [40]. In spite of this, our results suggests that different mechanisms could regulate survivin expression in canine OSA.…”

Section: Discussionsupporting

confidence: 81%

“…One of the most important aspects of the study of survivin expression in cancer is related to its high cancer specificity and consequent potential role as therapeutic target [37,38]. Survivin has been identified as a target gene of the β-catenin pathway [39], and it acts as a cell cycle regulator and apoptosis inhibitor, even if different isoforms with different functions of the molecule have been described [40]. …”

Section: Introductionmentioning

confidence: 99%

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Immunohistochemical investigation of cell cycle and apoptosis regulators (Survivin, β-Catenin, P53, Caspase 3) in canine appendicular osteosarcoma

et al. 2012

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BackgroundOsteosarcoma (OSA) represents the most common canine primary bone tumour. Despite several pathways have been investigated so far, few molecules have been identified as prognostic tools or potential therapeutic targets, and there is still the need to find out molecular pathways with specific influence over OSA progression to facilitate earlier prognosis and treatment.Aims of the present study were to evaluate the immunohistochemical pattern and levels of expression of a panel of molecules (survivin, β-catenin, caspase 3 -inactive and active forms- and p53) involved in cell cycle and apoptosis regulation in canine OSA samples, known to be of interest in the study also of human OSA, and to detect specific relations among them and with histological tumour grade, disease free interval (DFI) and overall survival (OS).ResultsNuclear β-catenin immunostaining was detected in normal osteoblasts adjacent to the tumour, and in 47% of the cases. Cytoplasmic and/or membranous immunostaining were also observed. Nuclear survivin and p53 positive cells were found in all cases. Moderate/high cytoplasmic β-catenin expression (≥10% positive cells) was significantly associated with the development of metastasis (P = 0.014); moderate/high nuclear p53 expression (≥10% positive cells) was significantly associated with moderate/high histological grade (P = 0.017) and shorter OS (P = 0.049). Moderate/high nuclear survivin expression (≥15% positive cells) showed a tendency toward a longer OS (P = 0,088).ConclusionsThe present results confirmed p53 as negative prognostic marker, while suggested survivin as a potential positive prognostic indicator, rather than indicative of a poor prognosis. The detection of nuclear β-catenin immunostaining in normal osteoblasts and the absent/low expression in most of the OSAs, suggested that this pathway could not play a major role in oncogenic transformation of canine osteoblasts. Further studies are needed to confirm these hypotheses.

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Section: Discussionsupporting

confidence: 81%

Section: Introductionmentioning

confidence: 99%

Immunohistochemical investigation of cell cycle and apoptosis regulators (Survivin, β-Catenin, P53, Caspase 3) in canine appendicular osteosarcoma

et al. 2012

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“…Similarly to the proliferation marker Ki-67 (Gilhar et al , 2004), N-surv-positive cells are more numerous in the epidermis from young individuals than from adult individuals. However, not all N-surv-expressing cells stain for Ki-67 in human cancerous skin (Bongiovanni et al , 2011). In addition, in the normal skin, Ki-67-positive cells are usually located in the basal layer of normal epidermis, whereas N-surv-positive cells are also detected in suprabasal layers.…”

Section: Discussionmentioning

confidence: 99%

Expression of nuclear survivin in normal skin and squamous cell carcinoma: a possible role in tumour invasion

et al. 2013

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Background:Survivin is detected in few adult normal cells and it is highly expressed in cancer. Nuclear survivin facilitates cell cycle entry, whereas the mitochondrial pool protects cells from apoptosis. Survivin is overexpressed in keratinocyte stem cells (KSCs) and protects them from apoptosis.Methods:As KSCs are at the origin of squamous cell carcinoma (SCC), we evaluated survivin expression in normal and cancerous skin in vivo by immunohistochemistry and western blotting. HaCaT cells overexpressing survivin and wound-healing assay are used. Analysis of variance and Student's T-tests are used for statistical analysis.Results:Survivin is localised in both the cytoplasm and nucleus of normal adult and young keratinocytes. Nuclear survivin is detected in one every 10 of 11 basal keratinocytes. When present in suprabasal cells, nuclear survivin is coexpressed with K10 but not with K15 or p75-neurotrophin receptor (p75NTR), a transit amplifying cell marker. Nuclear, but not cytoplasmic, survivin expression markedly increases in actinic keratosis and in SCC in situ, as compared with normal epidermis, and it is highest in poorly differentiated SCC. In SCC tumours, nuclear survivin-positive cells are mainly K10/p75NTR-negative and K15-positive. In poorly differentiated tumours, survivin mostly localises in the deep infiltrating areas. When overexpressed in keratinocytes, survivin increases cell migration.Conclusion:High survivin expression and the subcellular localisation of survivin correlate with keratinocyte differentiation and are associated with undifferentiated and more invasive SCC phenotype.

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“…In addition, there were 10 genes in the survivin network significantly up-regulated in PIS compared to other tissues. Because survivin is an inhibitor of apoptosis [59], up-regulated expressions of genes in this network may render the cells more resistant to apoptosis, which may in turn facilitate persistent infection. Studies conducted by Zhang and Alexandersen [60] and Zhang et al [61] showed that declining rate of FMDV levels during early infection rather than the virus levels determined FMDV persistent infection.…”

Section: Discussionmentioning

confidence: 99%

Mechanisms of Foot-and-Mouth Disease Virus Tropism Inferred from Differential Tissue Gene Expression

et al. 2013

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Foot-and-mouth disease virus (FMDV) targets specific tissues for primary infection, secondary high-titer replication (e.g. foot and mouth where it causes typical vesicular lesions) and long-term persistence at some primary replication sites. Although integrin αVβ6 receptor has been identified as primary FMDV receptors in animals, their tissue distribution alone fails to explain these highly selective tropism-driven events. Thus, other molecular mechanisms must play roles in determining this tissue specificity. We hypothesized that differences in certain biological activities due to differential gene expression determine FMDV tropism and applied whole genome gene expression profiling to identify genes differentially expressed between FMDV-targeted and non-targeted tissues in terms of supporting primary infection, secondary replication including vesicular lesions, and persistence. Using statistical and bioinformatic tools to analyze the differential gene expression, we identified mechanisms that could explain FMDV tissue tropism based on its association with differential expression of integrin αVβ6 heterodimeric receptor (FMDV receptor), fibronectin (ligand of the receptor), IL-1 cytokines, death receptors and the ligands, and multiple genes in the biological pathways involved in extracellular matrix turnover and interferon signaling found in this study. Our results together with reported findings indicate that differences in (1) FMDV receptor availability and accessibility, (2) type I interferon-inducible immune response, and (3) ability to clear virus infected cells via death receptor signaling play roles in determining FMDV tissue tropism and the additional increase of high extracellular matrix turnover induced by FMDV infection, likely via triggering the signaling of highly expressed IL-1 cytokines, play a key role in the pathogenesis of vesicular lesions.

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Survivin in skin pathologies

Cited by 25 publications

References 149 publications

Immunohistochemical investigation of cell cycle and apoptosis regulators (Survivin, β-Catenin, P53, Caspase 3) in canine appendicular osteosarcoma

Immunohistochemical investigation of cell cycle and apoptosis regulators (Survivin, β-Catenin, P53, Caspase 3) in canine appendicular osteosarcoma

Expression of nuclear survivin in normal skin and squamous cell carcinoma: a possible role in tumour invasion

Mechanisms of Foot-and-Mouth Disease Virus Tropism Inferred from Differential Tissue Gene Expression

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