Downregulation of Survivin Is Associated With Reductions in TNF Receptors' mRNA and Protein and Alterations in Nuclear Factor Kappa B Signaling in Urothelial Cancer Cells

Takizawa, Bayan T.; Uchio, Edward; Cohen, Justin J.; Wheeler, Marcia A.; Weiß, Robert M.

doi:10.1080/07357900701600954

Cited by 13 publications

(10 citation statements)

References 23 publications

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“…Survivin knockdown induces polyploidy because survivin is, besides its function as inhibitor of apoptosis, an integral part of the chromosomal passenger complex, thereby regulating chromosome segregation and cytokinesis (32). In agreement with the results of this study, Ning et al and Takizawa et al showed apoptosis induction and an arrest in G2/M cell cycle phase after treatment of BCa cells with siRNAs targeted at survivin (29,33). …”

Section: Discussionsupporting

confidence: 93%

Simultaneous siRNA-mediated knockdown of antiapoptotic BCL2, Bcl-xL, XIAP and survivin in bladder cancer cells

Kunze

2012

Int J Oncol

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Bladder cancer (BCa) represents the ninth most common malignancy worldwide. Despite intensive treatment with surgery and chemotherapy the prognosis for BCa patients particularly at advanced stages is poor. The ability to evade apoptosis is a hallmark of cancer cells. Since the antiapoptotic genes BCL2, Bcl-xL, XIAP and survivin are frequently upregulated in BCa tissues, their combined siRNA-mediated knockdown might be more potent in decreasing BCa growth than the single inhibition of one target. Against each target two siRNAs were selected that specifically reduced the mRNA and protein levels of their appropriate target in EJ28 and J82 BCa cells. Inhibition of survivin provoked the strongest antiproliferative effect of all single target treatments, for example cell counts decreased by 50%. Simultaneous targeting of all four antiapoptotic genes downregulated expression levels of all targets and mediated significant reductions in cell viability and cell counts as well as induction of apoptosis. In EJ28 cells, combined knockdown of BCL2, Bcl-xL, XIAP and survivin caused a 2.5-fold enhancement in apoptosis rate and reduced cellular viability by 40%. Therefore, simultaneous knockdown of antiapoptotic BCL2, Bcl-xL, XIAP and survivin may represent a promising treatment option for bladder cancer.

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Section: Discussionsupporting

confidence: 93%

Simultaneous siRNA-mediated knockdown of antiapoptotic BCL2, Bcl-xL, XIAP and survivin in bladder cancer cells

Kunze

2012

Int J Oncol

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“…35 ± 5.24% for Panc-1 and BxPC3, respectively (P \ 0.05), compared with the control groups, while there was no difference between the blank control and negative control groups survivin may play an important role in the development of pancreatic cancer. Takizawa et al [32] showed that the downregulation of survivin causes changes in mitosis and apoptosis, which may be related to changes in TNF receptors and NF-jB signaling.…”

Section: Discussionmentioning

confidence: 98%

siRNA Directed Against Survivin Enhances Pancreatic Cancer Cell Gemcitabine Chemosensitivity

et al. 2008

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Survivin is known to be overexpressed in various human malignancies, including pancreatic cancer, and to cause resistance to radiation and chemotherapy, so the regulation of this molecule could be a new strategy for treating pancreatic cancer. In our study, a short interfering RNA (siRNA) plasmid expression vector against survivin was constructed and transfected into human pancreatic cancer cell lines of Panc-1 and BxPC3. The expression of survivin mRNA and protein among the stable transfected cells and the untransfected cells was detected by semi-quantitative reverse transcriptase polymerase chain reaction (RT-PCR) and Western blot, respectively. Tumor cell growth in vitro was assessed by trypan blue exclusion. The cell cycle distribution and cell apoptosis were measured by flow cytometry. The cytotoxicity assay was measured by the MTT test. Our results showed that survivin siRNA treatment caused a specific and profound decrease of survivin mRNA and protein that was associated with decreased cell growth, spontaneous apoptosis, and a specific G0/G1 arrest. Furthermore, the suppression of survivin can enhance the chemosensitivity of pancreatic cancer cells to gemcitabine significantly. We suggest that the RNAi against survivin gene strategy would be a potential approach to chemosensitization therapy in human pancreatic cancer.

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“…Moreover, it is known to be overexpressed and related with more aggressive behavior, increased tumor recurrence, chemotherapy resistance, increased survival in various tumors [3][4][5][6][10][11][12][13][14][15]. In TC, Haghpanah et al reported the significantly higher survivin expression in TC than in follicular adenoma, and Ito et al reported the significant link between survivin expression and the dedifferentiation of TC [16,17].…”

Section: Discussionmentioning

confidence: 99%

Significance of survivin, caspase-3, and VEGF expression in thyroid carcinoma

Zhang

Meng

et al. 2009

Clin Exp Med

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To investigate the clinical significance of survivin, caspase-3, and vascular endothelial growth factor expression in a subset of thyroid carcinoma and their correlation with prognosis. Sixty-eight cases of thyroid carcinoma (TC), 12 cases of thyroid adenoma (TA) and 10 cases of normal thyroid tissue (NT) were involved in immunohistochemical and real-time RT-PCR analyses for survivin, caspase-3, and VEGF expression. Statistical analyses were performed for differential expression among NT, TA and TC, correlations of their expression with the clinicopathological parameters of TC including histological typing, clinical staging and lymphnode metastasis, and relationship of survivin with caspase-3 or VEGF in TC. We observed higher mRNA expression and positive immunostaining for survivin and VEGF in TC compared with TA and NT, with a significant positive correlation among them and significant correlations with histological typing, clinical staging and lymphnode metastasis in TC, but we could not find any significance of caspase-3 in TC and its significant relationship with survivin expression. Our results indicate that survivin and VEGF are unfavorable molecules for TC evolution and prognosis, and possess positive correlation in TC.

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Downregulation of Survivin Is Associated With Reductions in TNF Receptors' mRNA and Protein and Alterations in Nuclear Factor Kappa B Signaling in Urothelial Cancer Cells

Cited by 13 publications

References 23 publications

Simultaneous siRNA-mediated knockdown of antiapoptotic BCL2, Bcl-xL, XIAP and survivin in bladder cancer cells

Simultaneous siRNA-mediated knockdown of antiapoptotic BCL2, Bcl-xL, XIAP and survivin in bladder cancer cells

siRNA Directed Against Survivin Enhances Pancreatic Cancer Cell Gemcitabine Chemosensitivity

Significance of survivin, caspase-3, and VEGF expression in thyroid carcinoma

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