Increased Expression of Apoptosis Inhibitor Protein XIAP Contributes to Anoikis Resistance of Circulating Human Prostate Cancer Metastasis Precursor Cells

Berezovskaya, Olga; Schimmer, Aaron D.; Glinskii, Anna B.; Pinilla, Clemencia; Hoffman, Robert M.; Reed, John C.; Glinsky, Gennadi V.

doi:10.1158/0008-5472.can-04-2649

Cited by 218 publications

(193 citation statements)

References 38 publications

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“…Chang and colleagues using model systems showed that around 1×10 6 tumor cells per gram tumor tissue could be introduced daily into the blood stream (Chang et al, 2000). Though 85% CTCs become broken and disappear within 5 minutes, they still could be vital contributors of serum miRNA 200c (Berezovskaya et al, 2005). In other words, higher level of miRNA 200c may represent more tumor cells entering the circulation.…”

Section: Discussionmentioning

confidence: 99%

How to Explain the Contradiction of microRNA 200c Expression and Survival in Solid Tumors?: a Meta-analysis

Wang

Shen²,

Jiang³

et al. 2014

Asian Pacific Journal of Cancer Prevention

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Section: Discussionmentioning

confidence: 99%

How to Explain the Contradiction of microRNA 200c Expression and Survival in Solid Tumors?: a Meta-analysis

Wang

Shen²,

Jiang³

et al. 2014

Asian Pacific Journal of Cancer Prevention

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“…Finally, according to the recent studies, variants of prostate carcinoma cells selected for increased metastatic capacity displayed elevated levels of XIAP expression and anoikis resistance when compared to their parental poorly metastatic counterparts. Inhibition of XIAP expression in these cells resulted in the suppression of their anoikis resistance and the ability to metastasize (Berezovskaya et al, 2005).…”

Section: Discussionmentioning

confidence: 99%

“…Fifth, nontumorigenic anoikis-susceptible epithelial cells selected for increased anoikis resistance were found to be tumorigenic in vivo (Rak et al, 1999). Finally, treatment resulting in the inhibition of anoikis resistance of diverse types of tumor cells was shown to suppress their in vivo tumorigenicity (Rosen et al, 1998(Rosen et al, , 2000Scotlandi et al, 2002;Duxbury et al, 2004b) and the ability to metastasize (Scotlandi et al, 2002;Duxbury et al, 2004a, b;Jiang et al, 2004;Berezovskaya et al, 2005). For example, we found that ras oncogene blocks anoikis of intestinal epithelial cells by downregulating a proapoptotic protein Bak (Rosen et al, 1998) and by upregulating an antiapoptotic protein Bcl-X L (Rosen et al, 2000).…”

Section: Introductionmentioning

confidence: 99%

Detachment-induced upregulation of XIAP and cIAP2 delays anoikis of intestinal epithelial cells

Liu

et al. 2006

Oncogene

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Detachment of normal epithelial cells from the extracellular matrix triggers apoptosis, a phenomenon called anoikis. Conversely, carcinoma cells tend to be relatively more anoikis-resistant than their normal counterparts, and this increased resistance represents a critical feature of the malignant phenotype. Mechanisms that control susceptibility and resistance to anoikis are not fully understood. It is now known that detachment of non-malignant epithelial cells triggers both pro-and antiapoptotic signals, and it is the balance between these signals and the duration of detachment that determine further fate of the cells. Detachment-induced antiapoptotic events delay anoikis and if cells reattach relatively soon after detachment they survive. Direct regulators of apoptosis responsible for this delay of anoikis are unknown. We found that detachment of non-malignant intestinal epithelial cells triggers upregulation of inhibitors of apoptosis protein (IAP) family, such as X-chromosome-linked inhibitor of apoptosis protein and cellular inhibitor of apoptosis-2 (cIAP2). We demonstrated that this upregulation requires detachmentdependent activation of the transcription factor nuclear factor-jB. We further observed that various IAP antagonists accelerate anoikis, indicating that upregulation of the IAPs delays detachment-triggered apoptosis. We conclude that the IAPs are important regulators of the balance between detachment-triggered life and death signals. Perhaps, not by coincidence, these proteins are often upregulated in carcinomas, tumors composed of cells that tend to be anoikis-resistant.

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“…[10][11][12][13][14][15][16] Increased XIAP levels have been linked to escaping anoikis and apoptosis induced by radiation, chemotherapy and death receptor ligands. 13,[17][18][19][20][21][22] Furthermore, antagonism of XIAP has been reported to have antitumor activity in a number of models, including prostate cancer. 21,[23][24][25] Consistent with an antiapoptotic role, high levels of XIAP have an adverse prognosis in certain cancers.…”

mentioning

confidence: 99%

X-linked inhibitor of apoptosis deficiency in the TRAMP mouse prostate cancer model

et al. 2008

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Deregulation of apoptotic pathways plays a central role in cancer pathogenesis. X-linked inhibitor of apoptosis protein (XIAP), is an antiapoptotic molecule, whose elevated expression has been observed in tumor specimens from patients with prostate carcinoma. Studies in human cancer cell culture models and xenograft tumor models have demonstrated that loss of XIAP sensitizes cancer cells to apoptotic stimuli and abrogates tumor growth. In view of these findings, XIAP represents an attractive antiapoptotic therapeutic target for prostate cancer. To examine the role of XIAP in an immunocompetent mouse cancer model, we have generated transgenic adenocarcinoma of the mouse prostate (TRAMP) mice that lack XIAP. We did not observe a protective effect of Xiap deficiency in TRAMP mice as measured by tumor onset and overall survival. In fact, there was an unexpected trend toward more aggressive disease in the Xiap-deficient mice. These findings suggest that alternative mechanisms of apoptosis resistance are playing a significant oncogenic role in the setting of Xiap deficiency. Our study has implications for XIAP-targeting therapies currently in development. Greater understanding of these mechanisms will aid in combating resistance to XIAP-targeting treatment, in addition to optimizing selection of patients who are most likely to respond to such treatment. Cell Death and Differentiation (2008) Apoptosis is a process of cell death that is tightly regulated by a cadre of both pro-and antiapoptotic proteins. In contrast to healthy cells, a hallmark of cancerous cells is the acquired capacity to evade this process of programmed cell death. 1,2 The acquisition of genetic lesions leading to oncogene activation normally triggers a program of apoptosis or senescence. Additionally, the tumor microenvironment often exposes malignant cells to apoptotic stimuli, such as hypoxia or activation of death receptors. Thus, suppression of the pathway leading to cell death has been suggested as a necessarily early event in the development of neoplasia.Execution of the apoptotic cell death process is carried out by caspases, a family of cysteine aspartate proteases. 3,4 During apoptosis, loss of mitochondrial integrity or engagement of death receptors leads to the activation of initiator caspase-9 or -8, respectively. In either case, the initiator caspases cleave and activate effector caspases, including caspase-3 or -7. The cascade of caspase cleavage is regulated by X-linked inhibitor of apoptosis protein (XIAP). XIAP belongs to the IAP family, characterized by containing at least one zinc-binding baculovirus IAP repeat. 5 The only member of the IAP family that potently inhibits caspase activity, XIAP has been demonstrated to directly inhibit caspases-3, -7 and -9, blocking both intrinsic and extrinsic apoptotic signals. 6 Given its role in apoptosis, there has been much interest in understanding the role of XIAP in cancer and evaluating XIAP as a therapeutic target. [7][8][9] XIAP overexpression has been reported in a variety of human ca...

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Increased Expression of Apoptosis Inhibitor Protein XIAP Contributes to Anoikis Resistance of Circulating Human Prostate Cancer Metastasis Precursor Cells

Cited by 218 publications

References 38 publications

How to Explain the Contradiction of microRNA 200c Expression and Survival in Solid Tumors?: a Meta-analysis

How to Explain the Contradiction of microRNA 200c Expression and Survival in Solid Tumors?: a Meta-analysis

Detachment-induced upregulation of XIAP and cIAP2 delays anoikis of intestinal epithelial cells

X-linked inhibitor of apoptosis deficiency in the TRAMP mouse prostate cancer model

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