Bifunctional roles of survivin-ΔEx3 and survivin-2B for susceptibility to apoptosis in endometrial carcinomas

Tazo, Yuki; Hara, Atsuko; Onda, Takashi; Saegusa, Makoto

doi:10.1007/s00432-014-1762-8

Cited by 12 publications

(6 citation statements)

References 40 publications

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“…[36] In this study, the AIs detected by specific nuclear features in HE-stained sections were positively correlated with TUNEL positivity, in line with our previous data. [37] In agreement with other studies, [20,21] In conclusion, the present study provides evidence that Ps lesions within GBM may serve as a specialized microenvironment by acting as a hypoxic niche, in which the HIF-1/pAkt axis is activated, in response to severe hypoxia and promote CSC features in GBM.…”

Section: Accepted Manuscriptsupporting

confidence: 90%

Hypoxia-mediated cancer stem cells in pseudopalisades with activation of hypoxia-inducible factor-1α/Akt axis in glioblastoma

et al. 2015

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Section: Accepted Manuscriptsupporting

confidence: 90%

Hypoxia-mediated cancer stem cells in pseudopalisades with activation of hypoxia-inducible factor-1α/Akt axis in glioblastoma

et al. 2015

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“…The survivin gene produces three alternatively spliced variants, including full length, delta Ex3 (∆Ex3), and 2B transcripts (Figure 4, [49]), which exhibit differential effects on the apoptotic process [50]. Several studies demonstrated the cytoprotective effects of survivin ΔEx3 variants inhibiting the apoptotic process [51]. In contrast, the presence of the survivin 2B isoforms was reported to confer pro-apoptotic properties on cancer cells [51].…”

Section: Impacts Of Alternative Splicing Events On Apoptosismentioning

confidence: 99%

“…Several studies demonstrated the cytoprotective effects of survivin ΔEx3 variants inhibiting the apoptotic process [51]. In contrast, the presence of the survivin 2B isoforms was reported to confer pro-apoptotic properties on cancer cells [51]. Accordingly, relatively high expressions of full length and survivin ∆Ex3 variants are especially correlated with the active progression or poor prognoses of breast, gastric, thyroid, and pituitary cancers [52].…”

Section: Impacts Of Alternative Splicing Events On Apoptosismentioning

confidence: 99%

Differential Impacts of Alternative Splicing Networks on Apoptosis

Lin

Tsao

Lin

2016

IJMS

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Apoptosis functions as a common mechanism to eliminate unnecessary or damaged cells during cell renewal and tissue development in multicellular organisms. More than 200 proteins constitute complex networks involved in apoptotic regulation. Imbalanced expressions of apoptosis-related factors frequently lead to malignant diseases. The biological functions of several apoptotic factors are manipulated through alternative splicing mechanisms which expand gene diversity by generating discrete variants from one messenger RNA precursor. It is widely observed that alternatively-spliced variants encoded from apoptosis-related genes exhibit differential effects on apoptotic regulation. Alternative splicing events are meticulously regulated by the interplay between trans-splicing factors and cis-responsive elements surrounding the regulated exons. The major focus of this review is to highlight recent studies that illustrate the influences of alternative splicing networks on apoptotic regulation which participates in diverse cellular processes and diseases.

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“…Sustained overexpression of survivin has been shown to be cancer specific 7 - 9 . In addition, elevated expression of survivin plays a significant role in the inhibition of apoptosis 10 - 13 .These factors suggest that survivin is a potential therapeutic target 14 .…”

Section: Introductionmentioning

confidence: 99%

Silencing of Survivin Expression Leads to Reduced Proliferation and Cell Cycle Arrest in Cancer Cells

Zhou

et al. 2015

J. Cancer

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Survivin is an anti-apoptotic gene that is overexpressed in most human tumors. RNA interference using short interfering RNA (siRNA) can be used to specifically inhibit survivin expression. Tumor cells were treated with a newly designed survivin siRNA, which was modified with 2′-OMe. Cellular survivin mRNA and protein levels were determined by real-time qRT-PCR and Western blot, respectively. Cell cycle and apoptosis were determined by flow cytometry. Cell proliferation was measured by MTT assay. Our data showed that the novel survivin-targeted siRNA could efficiently knockdown the expression of survivin and inhibit cell proliferation. Survivin mRNA was reduced by 95% after 48h treatment with 20nM siRNA. In addition, the siRNA could markedly arrest the cell cycle at the G2/M checkpoint and induce cellular apoptosis in a dose-dependent manner. The percentage of apoptotic cells reached 50% when treated with 40nM siRNA. In conclusion, we have identified a novel chemically modified siRNA against survivin that is highly efficient and delineated its mechanism of action, thus demonstrating a potential therapeutic role for this molecule in cancer. Further evaluation of this siRNA for therapeutic activity is warranted.

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Bifunctional roles of survivin-ΔEx3 and survivin-2B for susceptibility to apoptosis in endometrial carcinomas

Abstract: These findings provided evidence that the balance among expression level of survivin variants may contribute to modulation of cell kinetics in Em Ca cells.

Cited by 12 publications

References 40 publications

Hypoxia-mediated cancer stem cells in pseudopalisades with activation of hypoxia-inducible factor-1α/Akt axis in glioblastoma

Hypoxia-mediated cancer stem cells in pseudopalisades with activation of hypoxia-inducible factor-1α/Akt axis in glioblastoma

Differential Impacts of Alternative Splicing Networks on Apoptosis

Silencing of Survivin Expression Leads to Reduced Proliferation and Cell Cycle Arrest in Cancer Cells

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