Reciprocal expression of survivin and SMAC/DIABLO in primary breast cancer

Mansour, Amal; Nabil, Mai M.; Ali-Labib, Randa; Said, Hazem; Annos, F.

doi:10.1007/s12032-011-0129-0

Cited by 8 publications

(6 citation statements)

References 42 publications

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“…51 Smac/DIABLO inhibits members of the IAP family, and overexpression of this protein was shown to potentiate the effectiveness of chemotherapy in breast cancer cells previously resistant to caspase-mediated apoptosis. 51 Specifically, Smac/DIABLO directly interacts with and inhibits XIAP. Conversely, overexpression of XIAP can repress the release of Smac/DIABLO from the mitochondria.…”

Section: Discussionmentioning

confidence: 99%

CDK4 inhibition and doxorubicin mediate breast cancer cell apoptosis through Smad3 and survivin

Tarasewicz¹,

Hamdan²,

Straehla³

et al. 2014

Cancer Biology & Therapy

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Cyclin D1/CDK4 activity is upregulated in up to 50% of breast cancers and CDK4-mediated phosphorylation negatively regulates the TGFβ superfamily member Smad3. We sought to determine if CDK4 inhibition and doxorubicin chemotherapy could impact Smad3-mediated cell/colony growth and apoptosis in breast cancer cells. Parental and cyclin D1-overexpressing MCF7 cells were treated with CDK4 inhibitor, doxorubicin, or combination therapy and cell proliferation, apoptosis, colony formation, and expression of apoptotic proteins were evaluated using an MTS assay, TUNEL staining, 3D Matrigel assay, and apoptosis array/immunoblotting. Study cells were also transduced with WT Smad3 or a Smad3 construct resistant to CDK4 phosphorylation (5M) and colony formation and expression of apoptotic proteins were assessed. Treatment with CDK4 inhibitor/doxorubicin combination therapy, or transduction with 5M Smad3, resulted in a similar decrease in colony formation. Treating cyclin D overexpressing breast cancer cells with combination therapy also resulted in the greatest increase in apoptosis, resulted in decreased expression of anti-apoptotic proteins survivin and XIAP, and impacted subcellular localization of pro-apoptotic Smac/DIABLO. Additionally, transduction of 5M Smad3 and doxorubicin treatment resulted in the greatest change in apoptotic protein expression. Collectively, this work showed the impact of CDK4 inhibitor-mediated, Smad3-regulated tumor suppression, which was augmented in doxorubicin-treated cyclin D-overexpressing study cells.

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Section: Discussionmentioning

confidence: 99%

CDK4 inhibition and doxorubicin mediate breast cancer cell apoptosis through Smad3 and survivin

Tarasewicz¹,

Hamdan²,

Straehla³

et al. 2014

Cancer Biology & Therapy

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“…Smac expression is more prevalent in the HER2 positive group than negative group (Zhang et al, 2011). Additonally, Smac mRNA expression is downregulated in breast cancer samples and shows an inverse correlation with survivin mRNA expression (Mansour et al, 2012).…”

Section: Breast Cancermentioning

confidence: 92%

DIABLO (diablo, IAP-binding mitochondrial protein)

Ceballos‐Cancino¹,

Meléndez-Zajgla²

2013

Atlas of Genetics and Cytogenetics in Oncology and Haematology

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“…Upstream factors, such as Smac released from mitochondria, inhibit IAPs by binding to the BIR structural domain, and there is evidence that survivin compromises apoptosis by suppressing caspase activator Smac. In addition, survivin also directly binds to and inhibits caspase-3 (Mansour et al, 2012 ). Through the above pathways, survivin alleviates the risk of cerebral hemorrhage after ischemic stroke by mitigating the destruction of the BBB triggered by apoptosis (Mallolas et al, 2014 ).…”

Section: The Role Of Sp1 In Ischemic Strokementioning

confidence: 99%

Specificity Protein 1: A Protein With a Two-Sided Role in Ischemic Stroke

Liu

Chen

et al. 2021

Front. Cell. Neurosci.

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Stroke is one of the leading causes of death and disability worldwide. However, there is a lack of effective medications to speed up the recovery process. Ischemic stroke, as the result of cerebral infarction or cerebral artery narrowing, is accompanied by hemiplegia or impaired consciousness. There are many transcription factors involved in the development of this condition, whose alterations can influence or signal the prognostic outcomes of ischemic stroke. Among them, the augmented expression of specificity protein 1 (SP1) can participate in the progression of the disease by binding DNA to regulate the transcriptions of many genes. Different studies have provided different answers as to whether SP1 plays a positive or a negative role in ischemic stroke. On the one hand, SP1 can play a cytoprotective role as both an antioxidant and anti-apoptotic agent for neurons and glial cells. On the other hand, it can also damage neuronal cells by promoting inflammation and exacerbating brain edema. In this review, we highlight the roles of SP1 in ischemic stroke and shed light on the underlying mechanism.

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Reciprocal expression of survivin and SMAC/DIABLO in primary breast cancer

Cited by 8 publications

References 42 publications

CDK4 inhibition and doxorubicin mediate breast cancer cell apoptosis through Smad3 and survivin

CDK4 inhibition and doxorubicin mediate breast cancer cell apoptosis through Smad3 and survivin

DIABLO (diablo, IAP-binding mitochondrial protein)

Specificity Protein 1: A Protein With a Two-Sided Role in Ischemic Stroke

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