The transcriptional induction of PIK3CA in tumor cells is dependent on the oncoprotein Y-box binding protein-1

Astanehe, Arezoo; Finkbeiner, M R; Hojabrpour, Payman; To, Karen; Fotovati, Abbas; Shadeo, Ashleen; Stratford, Anna L.; Lam, Wan L.; Berquin, Isabelle M.; Duronio, Vincent; Dunn, Sandra E.

doi:10.1038/onc.2009.81

Cited by 70 publications

(62 citation statements)

References 42 publications

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“…However, compared with ERK signaling, less attention has been paid to YB-1 as a therapeutic target. Nonetheless, YB-1 appears to be a more promising therapeutic target because, as a nodal factor, YB-1 regulates several factors possessing cancer-promoting functions, such as PCNA, EGFR, DNA topoisomerase II (7), CD44 (8), PIK3CA (9), and MET (10).…”

Section: Discussionmentioning

confidence: 99%

“…As a transcription factor in nucleus (6), YB-1 regulates the expression of various genes, including proliferating cell nuclear antigen (PCNA), EGF receptor (EGFR), DNA topoisomerase II (7), CD44 (8), phosphatidylinositol-4,5-bisphosphate 3-kinase, catalytic subunit alpha (PIK3CA; ref. 9), and MET (10). As well, YB-1 was shown to regulate gene expression at a translational level (11).…”

Section: Introductionmentioning

confidence: 99%

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Mutual Regulation between Raf/MEK/ERK Signaling and Y-Box–Binding Protein-1 Promotes Prostate Cancer Progression

Imada

Shiota

Kohashi

et al. 2013

Clinical Cancer Research

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Purpose: Y-box-binding protein-1 (YB-1) is known to conduct various functions related to cell proliferation, anti-apoptosis, epithelial-mesenchymal transition, and castration resistance in prostate cancer. However, it is still unknown how YB-1 affects cancer biology, especially its correlations with the mitogen-activated protein kinase (MAPK) signaling pathway. Therefore, we aimed to examine the interaction between YB-1 and the MAPK pathway in prostate cancer.Experimental Design: Quantitative real-time PCR, Western blotting, and co-immunoprecipitation assay were conducted in prostate cancer cells. YB-1, phosphorylated YB-1 (p-YB-1), and ERK2 protein expressions in 165 clinical specimens of prostate cancer were investigated by immunohistochemistry. YB-1, p-YB-1, and ERK2 nuclear expressions were compared with clinicopathologic characteristics and patient prognoses.Results: EGF upregulated p-YB-1, whereas MEK inhibitor (U0126, PD98059) decreased p-YB-1. Inversely, silencing of YB-1 using siRNA decreased the expression of ERK2 and phosphorylated MEK, ERK1/2, and RSK. Furthermore, YB-1 interacted with ERK2 and Raf-1 and regulated their expressions, through the proteasomal pathway. Immunohistochemical staining showed a significant correlation among the nuclear expressions of YB-1, p-YB-1, and ERK2. The Cox proportional hazards model revealed that high ERK2 expression was an independent prognostic factor [HR, 7.947; 95% confidence interval (CI), 3.527-20.508; P < 0.0001].Conclusion: We revealed the functional relationship between YB-1 and MAPK signaling and its biochemical relevance to the progression of prostate cancer. In addition, ERK2 expression was an independent prognostic factor. These findings suggest that both the ERK pathway and YB-1 may be promising molecular targets for prostate cancer diagnosis and therapeutics.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Mutual Regulation between Raf/MEK/ERK Signaling and Y-Box–Binding Protein-1 Promotes Prostate Cancer Progression

Imada

Shiota

Kohashi

et al. 2013

Clinical Cancer Research

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“…114 The same argument applies to other Y/CCAAT promoters, which YB-1 was shown to activate, including DNA Pola, 115 cyclin A, cyclin B1, 116 where many reports have also demonstrated an NF-Y dependence (Farina et al 117 ; reviewed in Gurtner et al 118 ). For other YB-1 targets, such as EGFR, PIK3CA, MET and CD44, [119][120][121][122] the Y/CCAAT, as it has been characterized genetically and bioinformatically, is absent.…”

Section: Nf-y Is the Sequence-specific Ccaat Factormentioning

confidence: 99%

Targeting the Y/CCAAT box in cancer: YB-1 (YBX1) or NF-Y?

Dolfini

Mantovani

2013

Cell Death Differ

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The Y box is an important sequence motif found in promoters and enhancers containing a CCAAT box -one of the few elements enriched in promoters of large sets of genes overexpressed in cancer. The search for the transcription factor(s) acting on it led to the biochemical purification of the nuclear factor Y (NF-Y) heterotrimer, and to the cloning -through the screening of expression libraries -of Y box-binding protein 1 (YB-1), an oncogene, overexpressed in aggressive tumors and associated with drug resistance. These two factors have been associated with Y/CCAAT-dependent activation of numerous growth-related genes, notably multidrug resistance protein 1. We review two decades of data indicating that NF-Y ultimately acts on Y/CCAAT in cancer cells, a notion recently confirmed by genome-wide data. Other features of YB-1, such as post-transcriptional control of mRNA biology, render it important in cancer biology.

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“…TFF secretory protein may have a role in bone metastasis in breast cancer [79], [80]. Genes encoding Y-box binding protein-1 (YB-1) [81], [82], [83] and C-myb [86] are oncogenes, while altered expression of oestrogen receptor (ER) [84], [87] and RSU-1/ RSP-1 [85] have been shown to critically influence the cellular proliferation and cell-cycle regulation in breast cancer. Thus, our experimental procedure is able to find the genes that are relevant to the disease and can facilitate early discovery as well as prognostic and therapeutic diversification of cancer patients.…”

Section: Biological Relevance Of the Selected Genesmentioning

confidence: 99%

Cancer Classification from Gene Expression Data by NPPC Ensemble

Ghorai

Mukherjee

Sengupta

et al. 2011

IEEE/ACM Trans. Comput. Biol. and Bioinf.

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Abstract-The most important application of microarray in gene expression analysis is to classify the unknown tissue samples according to their gene expression levels with the help of known sample expression levels. In this paper, we present a nonparallel plane proximal classifier (NPPC) ensemble that ensures high classification accuracy of test samples in a computer-aided diagnosis (CAD) framework than that of a single NPPC model. For each data set only, a few genes are selected by using a mutual information criterion. Then a genetic algorithm-based simultaneous feature and model selection scheme is used to train a number of NPPC expert models in multiple subspaces by maximizing cross-validation accuracy. The members of the ensemble are selected by the performance of the trained models on a validation set. Besides the usual majority voting method, we have introduced minimum average proximity-based decision combiner for NPPC ensemble. The effectiveness of the NPPC ensemble and the proposed new approach of combining decisions for cancer diagnosis are studied and compared with support vector machine (SVM) classifier in a similar framework. Experimental results on cancer data sets show that the NPPC ensemble offers comparable testing accuracy to that of SVM ensemble with reduced training time on average.

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The transcriptional induction of PIK3CA in tumor cells is dependent on the oncoprotein Y-box binding protein-1

Cited by 70 publications

References 42 publications

Mutual Regulation between Raf/MEK/ERK Signaling and Y-Box–Binding Protein-1 Promotes Prostate Cancer Progression

Mutual Regulation between Raf/MEK/ERK Signaling and Y-Box–Binding Protein-1 Promotes Prostate Cancer Progression

Targeting the Y/CCAAT box in cancer: YB-1 (YBX1) or NF-Y?

Cancer Classification from Gene Expression Data by NPPC Ensemble

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