Survivin expression and targeting in breast cancer

Jha, Kaushal Kumar; Shukla, Manish; Pandey, Manoj

doi:10.1016/j.suronc.2011.01.001

Cited by 145 publications

(142 citation statements)

References 57 publications

Supporting

Mentioning

131

Contrasting

Unclassified

Order By: Relevance

“…The transcription factor GATA 1 that was found to upregulate survivin expression in breast carcinoma could be a novel target of therapy. A research group revealed that the extraction of the grape seed regulates the function of a transcription factor, which is associated with the core promoter of survivin and can finally reduce its activity [43] .…”

Section: Partnersmentioning

confidence: 99%

“…Survivin mRNA expression was inversely correlated with the sensitivity to ionizing radiation [43,47,48] . Additionally, survivin could be a radio resistance factor since its production was increased by sublethal doses of radiation [49] .…”

Section: Radiotherapy and Survivinmentioning

confidence: 99%

“…Additionally, survivin could be a radio resistance factor since its production was increased by sublethal doses of radiation [49] . Transfer of tumor-specific adenovirus-mediated PUMA gene using the survivin promoter enhances the radiosensitivity of breast cancer cells in vitro and in vivo [43] . Also, signal transducer and activator of transcription 3 (Stat 3) could be used as target therapy in sensitization by radiation for patients with breast carcinomas, because these two molecules influence survivin.…”

Section: Radiotherapy and Survivinmentioning

confidence: 99%

“…Also, signal transducer and activator of transcription 3 (Stat 3) could be used as target therapy in sensitization by radiation for patients with breast carcinomas, because these two molecules influence survivin. Radiotherapeutic sensitization approach has not been widely used in all clinical trials, despite the fact that survivin inhibitors might be a new group of antagonists, which might enhance the effects of radiotherapy when survivin is overexpressed [43,50] .…”

Section: Radiotherapy and Survivinmentioning

confidence: 99%

See 3 more Smart Citations

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

Pavlidou

Kroupis

Dimas

2014

WJCO

View full text Add to dashboard Cite

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

show abstract

Section: Partnersmentioning

confidence: 99%

Section: Radiotherapy and Survivinmentioning

confidence: 99%

Section: Radiotherapy and Survivinmentioning

confidence: 99%

Section: Radiotherapy and Survivinmentioning

confidence: 99%

See 2 more Smart Citations

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

Pavlidou

Kroupis

Dimas

2014

WJCO

View full text Add to dashboard Cite

show abstract

“…Survivin is an important member of IAPs and is expressed in majority of breast cancers. 21 Hence, we analyzed the effects of M-CSF on apoptosis in MCF-7 cells. We found that M-CSF-induced significant doxorubicin resistance of MCF-7 cell and the effect was mediated by apoptosis inhibition through activation of the PI3K/Akt/ Survivin pathway.…”

Section: Discussionmentioning

confidence: 99%

Doxorubicin resistance mediated by cytoplasmic macrophage colony-stimulating factor is associated with switch from apoptosis to autophagic cell death in MCF-7 breast cancer cells

Zhang

Tang

et al. 2016

Exp Biol Med (Maywood)

View full text Add to dashboard Cite

Macrophage colony-stimulating factor is a vital factor in maintaining the biological function of monocyte-macrophage lineage. It is expressed in many tumor tissues and cancer cells. Recent findings indicate that macrophage colony-stimulating factor might contribute to chemoresistance, but the precise mechanisms are unclear. This study was to explore the effect of macrophage colony-stimulating factor on doxorubicin resistance in MCF-7 breast cancer cells and the possible mechanism. In the study, the human breast cancer cells, MCF-7, were transfected with macrophage colony-stimulating factor. We document that cytoplasmic macrophage colony-stimulating factor induces doxorubicin resistance and inhibits apoptosis in MCF-7 cells. Further studies demonstrated that cytoplasmic macrophage colony-stimulating factor-mediated apoptosis inhibition was dependent on the activation of PI3K/Akt/Survivin pathway. More importantly, we found that macrophage colony-stimulating factor-induced autophagic cell death in doxorubicin-treated MCF-7 cells. Taken together, we show for the first time that macrophage colony-stimulating factor-induced doxorubicin resistance is associated with the changes in cell death response with defective apoptosis and promotion of autophagic cell death.

show abstract

A moderate static magnetic field enhances TRAIL‐induced apoptosis by the inhibition of Cdc2 and subsequent downregulation of survivin in human breast carcinoma cells

Lin

Wan

et al. 2014

Bioelectromagnetics

View full text Add to dashboard Cite

Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) exhibits its potent antitumor activity via membrane receptors on cancer cells without deleterious side effects for normal tissue. However, as many other cancer types, breast cancer cells develop a resistance to TRAIL. In the present study, we reported that exposure to 3.0 mT static magnetic field (SMF) mediated the sensitization of breast cancer cells to TRAIL-induced apoptosis. This effect was significantly reduced by the forced expression of survivin, suggesting the sensitization was mediated at least in part through the inhibition of survivin expression. In addition, SMF alone or in combination with TRAIL induced a cell cycle arrest within the G2 /M phase, and the reduction in the survivin protein level was associated with the downregulated expression of Cdc2, a cyclin B-dependent kinase that is necessary for the entry into the M phase. Taken together, our results demonstrated that SMF promoted TRAIL-induced apoptosis by inhibiting the expression of Cdc2 and, subsequently, survivin. Of note, SMF did not sensitize untransformed human mammary epithelial cells to TRAIL-mediated apoptosis. Therefore, the combined treatment of SMF and TRAIL may offer an attractive strategy for safely treating resistant breast cancers.

show abstract

Survivin expression and targeting in breast cancer

Cited by 145 publications

References 57 publications

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

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

Doxorubicin resistance mediated by cytoplasmic macrophage colony-stimulating factor is associated with switch from apoptosis to autophagic cell death in MCF-7 breast cancer cells

A moderate static magnetic field enhances TRAIL‐induced apoptosis by the inhibition of Cdc2 and subsequent downregulation of survivin in human breast carcinoma cells

Contact Info

Product

Resources

About