Biomarker expression patterns that correlate with high grade features in treatment naive, organ-confined prostate cancer

McDonnell, Timothy J.; Chari, Nikhil; Cho‐Vega, Jeong Hee; Troncoso, Patricia; Wang, Xuemei; Bueso‐Ramos, Carlos E.; Coombes, Kevin R.; Brisbay, Shawn; Lopez, Remigio; Prendergast, George C.; Logothetis, Christopher J.; Do, Kim‐Anh

doi:10.1186/1755-8794-1-1

Cited by 35 publications

(32 citation statements)

References 25 publications

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“…25 Subsequent loss of p53 leads to hyperproliferative phenotypes in several cancer cell lines. 26–28 Collectively these studies point toward an important influence of Pim-1 expression to increase cell cycling, but the role of Pim-1 on CPC proliferation has yet to be elucidated. To determine whether Pim-1 enhances CPC cycling, control nontransgenic mice (NTG) were compared to 3 genetically engineered mouse lines with altered Pim-1 activity: cardiac-specific overexpression of Pim-1 (Pim-wt), a kinase dead form of Pim-1 (Pim-DN), 9 and Pim-1–null mice (Pim-KO).…”

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confidence: 99%

Cardiac Progenitor Cell Cycling Stimulated by Pim-1 Kinase

Cottage

Bailey

Fischer

et al. 2010

Circulation Research

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Rationale Cardioprotective effects of Pim-1 kinase have been previously reported but the underlying mechanistic basis may involve a combination of cellular and molecular mechanisms that remain unresolved. The elucidation of the mechanistic basis for Pim-1 mediated cardioprotection provides important insights for designing therapeutic interventional strategies to treat heart disease. Objective Effects of cardiac-specific Pim-1 kinase expression on the cardiac progenitor cell (CPC) population were examined to determine whether Pim-1 mediates beneficial effects through augmenting CPC activity. Methods and Results Transgenic mice created with cardiac-specific Pim-1 overexpression (Pim-wt) exhibit enhanced Pim-1 expression in both cardiomyocytes and CPCs, both of which show increased proliferative activity assessed using 5-bromodeoxyuridine (BrdU), Ki-67, and c-Myc relative to nontransgenic controls. However, the total number of CPCs was not increased in the Pim-wt hearts during normal postnatal growth or after infarction challenge. These results suggest that Pim-1 overexpression leads to asymmetric division resulting in maintenance of the CPC population. Localization and quantitation of cell fate determinants Numb and α-adaptin by confocal microscopy were used to assess frequency of asymmetric division in the CPC population. Polarization of Numb in mitotic phospho-histone positive cells demonstrates asymmetric division in 65% of the CPC population in hearts of Pim-wt mice versus 26% in nontransgenic hearts after infarction challenge. Similarly, Pim-wt hearts had fewer cells with uniform α-adaptin staining indicative of symmetrically dividing CPCs, with 36% of the CPCs versus 73% in nontransgenic sections. Conclusions These findings define a mechanistic basis for enhanced myocardial regeneration in transgenic mice overexpressing Pim-1 kinase.

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confidence: 99%

Cardiac Progenitor Cell Cycling Stimulated by Pim-1 Kinase

Cottage

Bailey

Fischer

et al. 2010

Circulation Research

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“…Inguinal adipose tissue of mice fed high fat diet (HFD) was analyzed and Pcyt2 was found to be up-regulated in high fat gainers on HFD in comparison to low fat gainers on the same diet. Pcyt2 expression was also up-regulated in proximal and middle part of small intestine in mice fed high fat diet (HFD) for 2–8 weeks in comparison to the control animals fed low-fat diet [54]. Immunochemical analysis revealed that villi in the small intestine were enlarged in mice fed HFD.…”

Section: Pcyt2 Expression In the Metabolic Syndrome And Related DImentioning

confidence: 99%

“…Immunochemical analysis revealed that villi in the small intestine were enlarged in mice fed HFD. In these mice, the number of cells per villus and body length was higher, a characteristics that may function to extend the capacity of lipid absorption [54]. Increased cell proliferation requires increased phospholipid synthesis which could explain up-regulation of Pcyt2 expression.…”

Section: Pcyt2 Expression In the Metabolic Syndrome And Related DImentioning

confidence: 99%

Regulation of Phosphatidylethanolamine Homeostasis — The Critical Role of CTP:Phosphoethanolamine Cytidylyltransferase (Pcyt2)

Pavlovic

Bakovic

2013

IJMS

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Phosphatidylethanolamine (PE) is the most abundant lipid on the protoplasmatic leaflet of cellular membranes. It has a pivotal role in cellular processes such as membrane fusion, cell cycle regulation, autophagy, and apoptosis. CTP:phosphoethanolamine cytidylyltransferase (Pcyt2) is the main regulatory enzyme in de novo biosynthesis of PE from ethanolamine and diacylglycerol by the CDP-ethanolamine Kennedy pathway. The following is a summary of the current state of knowledge on Pcyt2 and how splicing and isoform specific differences could lead to variations in functional properties in this family of enzymes. Results from the most recent studies on Pcyt2 transcriptional regulation, promoter function, autophagy, and cell growth regulation are highlighted. Recent data obtained from Pcyt2 knockout mouse models is also presented, demonstrating the essentiality of this gene in embryonic development as well as the major physiological consequences of deletion of one Pcyt2 allele. Those include development of symptoms of the metabolic syndrome such as elevated lipogenesis and lipoprotein secretion, hypertriglyceridemia, liver steatosis, obesity, and insulin resistance. The objective of this review is to elucidate the nature of Pcyt2 regulation by linking its catalytic function with the regulation of lipid and energy homeostasis.

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“…Although the causal relationship between inflammation, innate immunity and cancer is more widely accepted, many of the molecular and cellular mechanisms mediating this relationship remain unresolved (Coussens and Werb, 2002). Many studies have implicated Nrf2 (Nfe2l2) in cancer (Ramos-Gomez et al, 2001;Katsuoka et al, 2005;Sporn and Liby, 2005;Nair et al, 2007a;Pearson et al, 2008) or inflammation-associated diseases such as colitis (Khor et al, 2006;Osburn et al, 2007), and Parkinson's disease (Clements et al, 2006), and NF-kB in inflammation (Muller-Ladner et al, 2002;Profita et al, 2008;Puthia et al, 2008) and cancer Cilloni et al, 2006;Sun and Zhang, 2007;McDonnell et al, 2008). Indeed, the identification of combinatorial, or synergistic, transcription factors and the elucidation of relationships among them are of great importance for understanding transcriptional regulation as well as transcription factor networks (Hu et al, 2007).…”

Section: A Putative Model For Nrf2 -Nfkb1 Interactions In Inflammatiomentioning

confidence: 99%

Regulatory potential for concerted modulation of Nrf2- and Nfkb1-mediated gene expression in inflammation and carcinogenesis

et al. 2008

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Many studies have implicated nuclear factor E2-related factor 2 (Nrf2) and nuclear factor-kB1 (Nfkb1) in inflammation and cancer. However, the regulatory potential for crosstalk between these two important transcription factors in inflammation and carcinogenesis has not been explored. To delineate conserved transcription factor-binding site signatures, we performed bioinformatic analyses on the promoter regions of human and murine Nrf2 and Nfkb1. We performed multiple sequence alignment of Nrf2 and Nfkb1 genes in five mammalian species -human, chimpanzee, dog, mouse and rat -to explore conserved biological features. We constructed a canonical regulatory network for concerted modulation of Nrf2 and Nfkb1 involving several members of the mitogen-activated protein kinase (MAPK) family and present a putative model for concerted modulation of Nrf2 and Nfkb1 in inflammation/ carcinogenesis. Our results reflect potential for putative crosstalk between Nrf2 and Nfkb1 modulated through the MAPK cascade that may influence inflammation-associated etiopathogenesis of cancer. Taken together, the elucidation of potential relationships between Nrf2 and Nfkb1 may help to better understand transcriptional regulation, as well as transcription factor networks, associated with the etiopathogenesis of inflammation and cancer.

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Biomarker expression patterns that correlate with high grade features in treatment naive, organ-confined prostate cancer

Cited by 35 publications

References 25 publications

Cardiac Progenitor Cell Cycling Stimulated by Pim-1 Kinase

Cardiac Progenitor Cell Cycling Stimulated by Pim-1 Kinase

Regulation of Phosphatidylethanolamine Homeostasis — The Critical Role of CTP:Phosphoethanolamine Cytidylyltransferase (Pcyt2)

Regulatory potential for concerted modulation of Nrf2- and Nfkb1-mediated gene expression in inflammation and carcinogenesis

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