Survivin prevents apoptosis by binding to caspase-3 in astrocytes infected with the BeAn strain of Theiler’s murine encephalomyelitis virus

Rubio, Nazario; Garcia-Segura, Luis Miguel; Arévalo, María Ángeles

doi:10.1007/s13365-012-0112-3

Cited by 14 publications

(13 citation statements)

References 37 publications

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“…Wee1 has been reported to inhibit CDK1 activity by phosphorylation (Chow and Poon, 2012;Magnussen et al, 2012), which in turn decreases survivin (Chen et al, 2013) and consequently activates Caspase-3 (Jones et al, 2010;Rubio et al, 2012). The phosphorylation of CDK1 and decrease in survivin are also involved in the mechanism of apoptosis via mitotic catastrophe (Castedo et al, 2004;Lamers et al, 2011).…”

Section: Discussionmentioning

confidence: 99%

Involvement of Wee1 in the Circadian Rhythm–Dependent Intestinal Damage Induced by Docetaxel

Obi-Ioka¹,

Ushijima²,

Kusama³

et al. 2013

J Pharmacol Exp Ther

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Docetaxel, a semisynthetic taxane, is effective for the treatment of some solid cancers; however, docetaxel-induced intestinal damage leads to poor prognosis in some patients. Although such adverse effects have been reported to depend on the dosing-time of docetaxel, the mechanisms involved remain unclear. Wee1 expression is controlled by the clock gene complex, clock/bmal1, and contributes to cell-cycle progression. The present study was undertaken to evaluate the potential role of Wee1 in the circadian rhythm-dependent profile of docetaxel. Male mice were maintained under a 12-hour light/ dark cycle. Intestinal damage after repeated dosing of docetaxel (20 mg/kg) for 3 weeks was more severe at 14 hours after light on (HALO) than at 2 HALO. The intestinal protein expressions of Wee1, phosphorylated CDK1, and cleaved Caspase-3 were higher in the 14-HALO group than in the 2-HALO group, whereas that of survivin was lower in the 14-HALO group. Thus, it is speculated that elevated Wee1 expression inhibited CDK1 activity more by phosphorylation, which in turn caused the lower expression of survivin and consequently more activated Caspase-3 in the 14-HALO group. There were no significant differences in plasma docetaxel concentrations between the 2-and 14-HALO groups. Bindings of CLOCK and BMAL1 to the E-box regions at the wee1 gene promoter were not altered by docetaxel treatment at 2 and 14 HALO. These findings suggest that Wee1 is directly or indirectly involved in the mechanism of the circadian rhythm-dependent changes in docetaxel-induced intestinal damage. However, the mechanism for a circadian rhythm-dependent change in intestinal Wee1 expression by docetaxel remains to be determined.

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Section: Discussionmentioning

confidence: 99%

Involvement of Wee1 in the Circadian Rhythm–Dependent Intestinal Damage Induced by Docetaxel

Obi-Ioka¹,

Ushijima²,

Kusama³

et al. 2013

J Pharmacol Exp Ther

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“…Interesting results were reported with the upregulation of survivin expression, where it formed a complex with the caspase-3 enzyme, nullifying the apoptotic events to be followed. 62 Supportive data also exist on the cytoprotective actions of dominant-negative survivin M34 against the DNA-damaging induced agents. 50,53 Given its protective potential, several mutant versions of wild-type survivin have been explored, of which the BIR-motif mutant known as dominant-negative survivin C84A was employed in this study.…”

Section: Proliferative Effects Of Surr9-c84amentioning

confidence: 98%

Nanoformulated cell-penetrating survivin mutant and its dual actions

Sriramoju¹,

Kanwar²,

Kanwar³

2014

IJN

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In this study, we investigated the differential actions of a dominant-negative survivin mutant (SurR9-C84A) against cancerous SK-N-SH neuroblastoma cell lines and differentiated SK-N-SH neurons. In both the cases, the mutant protein displayed dual actions, where its effects were cytotoxic toward cancerous cells and proliferative toward the differentiated neurons. This can be explained by the fact that tumorous (undifferentiated SK-N-SH) cells have a high endogenous survivin pool and upon treatment with mutant SuR9-C84A causes forceful survivin expression. These events significantly lowered the microtubule dynamics and stability, eventually leading to apoptosis. In the case of differentiated SK-N-SH neurons that express negligible levels of wild-type survivin, the mutant indistinguishably behaved in a wild-type fashion. It also favored cell-cycle progression, forming the chromosome-passenger complex, and stabilized the microtubule-organizing center. Therefore, mutant SurR9-C84A represents a novel therapeutic with its dual actions (cytotoxic toward tumor cells and protective and proliferative toward neuronal cells), and hence finds potential applications against a variety of neurological disorders. In this study, we also developed a novel poly(lactic- co -glycolic acid) nanoparticulate formulation to surmount the hurdles associated with the delivery of SurR9-C84A, thus enhancing its effective therapeutic outcome.

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“…Previous studies found that Bcl-2 enhances the anti-apoptotic ability of the tumor cells by regulating the mitochondrial redox state of thiol ( 14 ). Survivin inhibits caspase activation, and therefore leads to the negative regulation of programmed cell death ( 15 ). In summary, these results show that the expression of anti-apoptotic associated genes, Bcl-2 and survivin , was extremely reduced following the silencing of Znf139 .…”

Section: Discussionmentioning

confidence: 99%

Effects of ZNF139 on gastric cancer cells and mice with gastric tumors

Nie¹,

et al. 2016

Oncology Letters

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Gastric cancer (GC) is the fourth most common type of cancer, worldwide. The major molecular factors associated with the pathogenesis of GC remain unclear. Previous studies found that zinc finger proteins are highly abundant in human eukaryotes and tissues, and play an important role in maintaining normal cellular functions and have an association with tumor initiation. In the current study, interference technology was used to silence the ZNF139 protein, a zinc finger protein that was previously found to be closely associated with GC. The results showed that cell viability and proliferation were inhibited in the Znf139-knockdown of GC cells. Additional study found that the expression levels of B cell lymphoma-2 (Bcl-2) and survivin messenger RNAs and proteins were downregulated in Znf139-silenced cells, indicating that cells expression Znf139 are able to induce the growth of tumor cells by mediating the apoptosis pathway. Further in vivo experiments showed that Znf139 knockdown downregulated the expression levels of Bcl-2 and survivin in mice. Overall, the in vitro and in vivo findings of the present study indicate that ZNF139 may be actively involved in the progression of GC.

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Survivin prevents apoptosis by binding to caspase-3 in astrocytes infected with the BeAn strain of Theiler’s murine encephalomyelitis virus

Cited by 14 publications

References 37 publications

Involvement of Wee1 in the Circadian Rhythm–Dependent Intestinal Damage Induced by Docetaxel

Involvement of Wee1 in the Circadian Rhythm–Dependent Intestinal Damage Induced by Docetaxel

Nanoformulated cell-penetrating survivin mutant and its dual actions

Effects of ZNF139 on gastric cancer cells and mice with gastric tumors

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