Prognostic value of inhibitors of apoptosis proteins (IAPs) and caspases in prostate cancer: caspase-3 forms and XIAP predict biochemical progression after radical prostatectomy

Rodríguez-Berriguete, Gonzalo; Torrealba, Norelia; Ortega, Miguel Á.; Martínez-Onsurbe, Pilar; Olmedilla, Gabriel; Paniagua, Ricardo; Guil-Cid, Manuel; Fraile, Benito; Royuela, Mar

doi:10.1186/s12885-015-1839-z

Cited by 29 publications

(23 citation statements)

References 32 publications

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“…As key factors, caspases are involved in the initiation and execution of apoptosis [19]. Caspase-3 is a type of executioner caspase, which can proteolyze a lot of substrates causing the death of cell [20], while its direct inhibitor, X-linked inhibitor of apoptosis protein (XIAP), can prevent cell from apoptosis by suppressing caspase cascade [21]. Thus, XIAP/caspase-3 pathway may play an important role in radiotherapy-induced apoptosis.…”

Section: Introductionmentioning

confidence: 99%

α-bisabolol enhances radiotherapy-induced apoptosis in endometrial cancer cells by reducing the effect of XIAP on inhibiting caspase-3

Fang¹,

Wang²,

Li³

et al. 2019

Bioscience Reports

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Endometrial cancer (EC) is one of the most common cancers in females. Although the diagnosis and treatment in early stages can greatly improve the survival rate of patients, the advanced EC still is lethal. Radiotherapy is widely used against EC, and it is a great challenge to find an effective way to overcome the resistance of EC during radiotherapy. α-bisabolol is a promising drug, which has already exhibited its anti-tumor effect in some malignancies. Here we reported that α-bisabolol could inhibit the proliferation of EC cells. It is also shown that their abilities of migration and invasion were effectively reduced by α-bisabolol. Furthermore, our results also demonstrated that α-bisabolol could improve sensitivity of EC cells in radiotherapy and further inhibited the growth of EC cells. By Western blot, we found the expression of matrix metalloproteinases-9 (MMP-9) and cyclin E were significantly decreased, which indicated that EC cells can be further suppressed by using α-bisabolol and radiotherapy. It is also demonstrated in our study that the rate of apoptotic cells is markedly increased in EC by using these two treatments. The significant decrease in X-linked inhibitor of apoptosis protein (XIAP) and increase in caspase-3 detected in our study suggested that the enhancement of apoptosis is mediated by XIAP/caspase-3 pathway, which was further confirmed by examining the downstream effectors of caspase-3, COX-2, PARP and cleaved PARP. In the present study, we demonstrated that α-bisabolol could enhance the sensitivity of EC cells to radiotherapy, which provide a novel alternative for overcoming radioresistance of EC cells and achieving a better outcome in radiotherapy.

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Section: Introductionmentioning

confidence: 99%

α-bisabolol enhances radiotherapy-induced apoptosis in endometrial cancer cells by reducing the effect of XIAP on inhibiting caspase-3

Fang¹,

Wang²,

Li³

et al. 2019

Bioscience Reports

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“…[4][5][6] Survivin is largely undetectable in most normal, terminally differentiated tissues with notable exceptions of vascular endothelial or haematopoietic cells. [8][9][10] Moriai et al 11 recently showed that targeting survivin may overcome tamoxifen resistance in breast cancer cells. [8][9][10] Moriai et al 11 recently showed that targeting survivin may overcome tamoxifen resistance in breast cancer cells.…”

Section: Introductionmentioning

confidence: 99%

Lovastatin‐mediated MCF‐7 cancer cell death involves LKB1‐AMPK‐p38MAPK‐p53‐survivin signalling cascade

Huang

Chyuan

Shiue

et al. 2019

J Cellular Molecular Medi

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There is increasing evidence that statins, which are widely used in lowering serum cholesterol and the incidence of cardiovascular diseases, also exhibits anti-tumour properties. The underlying mechanisms by which statins-induced cancer cell death, however, remain incompletely understood. In this study, we explored the anti-tumour mechanisms of a lipophilic statin, lovastatin, in MCF-7 breast cancer cells. Lovastatin inhibited cell proliferation and induced cell apoptosis. Lovastatin caused p21 elevation while reduced cyclin D1 and survivin levels. Lovastatin also increased p53 phosphorylation, acetylation and its reporter activities. Results from chromatin immunoprecipitation analysis showed that p53 binding to the survivin promoter region was increased, while Sp1 binding to the region was decreased, in MCF-7 cells after lovastatin exposure. These actions were associated with liver kinase B1 (LKB1), AMP-activated protein kinase (AMPK) and p38 mitogen-activated protein kinase (p38MAPK) activation. Lovastatin's enhancing effects on p53 activation, p21 elevation and survivin reduction were significantly reduced in the presence of p38MAPK signalling inhibitor. Furthermore, LKB1-AMPK signalling blockade abrogated lovastatin-induced p38MAPK and p53 phosphorylation. Together these results suggest that lovastatin may activate LKB1-AMPK-p38MAPK-p53-survivin cascade to cause MCF-7 cell death. The present study establishes, at least in part, the signalling cascade by which lovastatin induces breast cancer cell death. K E Y W O R D Sbreast cancer, liver kinase B1, lovastatin, p53, surviving Huang and Chyuan contributed equally to this work. | 1823HUANG et Al.

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“…3A). These results suggest that CD164 may modulate NHA progression by increasing cell proliferation, which is considered to be associated with a significant decrease in the Bax/Bcl2 ratio (22). Cell viability was significantly increased in NHA cells overexpressing CD164 when compared with the vector control at 24, 48 and 72 h following transfection (P<0.01, P<0.001 and P<0.001, respectively; Fig.…”

Section: Resultsmentioning

confidence: 99%

“…Previous studies have indicated that the Bax/Bcl2 ratio is involved in the release of cytochrome c to the cytosol, resulting in caspase activation (21). In addition, overexpression of the anti-apoptotic Bcl2 protein protects cells from apoptosis induced by stimulants (22). The present study demonstrated that silencing of CD164 in U87 cells results in upregulation of cleaved caspase 3 and alters the Bax/Bcl2 ratio by increasing Bax and decreasing Bcl2 expression.…”

Section: Discussionmentioning

confidence: 99%

CD164 regulates proliferation and apoptosis by targeting PTEN in human glioma

Cai

Zheng

et al. 2017

Molecular Medicine Reports

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Cluster of differentiation 164 (CD164), a sialomucin, has been demonstrated to be involved in the regulation of proliferation, apoptosis, adhesion and differentiation in multiple cancers. CD164 is regarded to be a potential promotor of tumor growth. However, the involvement of CD164 in human glioma proliferation and apoptosis remains unknown. The aim of the present study was to investigate the expression and oncogenic function of CD164 in normal human astrocytes (NHA) and glioma cells in vitro and in vivo. The results of the present study demonstrated that CD164 mRNA and protein levels were significantly increased in human glioma cell lines and tissue samples. CD164 overexpression promoted the proliferation of NHA in vitro, and its tumorigenic effect was confirmed in a murine xenograft model. Knockdown of CD164 inhibited cell proliferation and promoted apoptosis of the U87 human glioma cell line in vitro and in vivo. In addition, knockdown of CD164 was demonstrated to upregulate the Bax/Bcl2 ratio and phosphatase and tensin homolog (PTEN) expression, reduce protein kinase B (AKT) phosphorylation and promote the expression of p53 in U87 cells. The results suggest that CD164 expression may have affected the proliferation and apoptosis of human glioma cells via the PTEN/phosphoinositide 3-kinase/AKT pathway, and may therefore present a potential target for the diagnosis and treatment of glioma.

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Prognostic value of inhibitors of apoptosis proteins (IAPs) and caspases in prostate cancer: caspase-3 forms and XIAP predict biochemical progression after radical prostatectomy

Cited by 29 publications

References 32 publications

α-bisabolol enhances radiotherapy-induced apoptosis in endometrial cancer cells by reducing the effect of XIAP on inhibiting caspase-3

α-bisabolol enhances radiotherapy-induced apoptosis in endometrial cancer cells by reducing the effect of XIAP on inhibiting caspase-3

Lovastatin‐mediated MCF‐7 cancer cell death involves LKB1‐AMPK‐p38MAPK‐p53‐survivin signalling cascade

CD164 regulates proliferation and apoptosis by targeting PTEN in human glioma

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