Expression of selenium‐binding protein 1 characterizes intestinal cell maturation and predicts survival for patients with colorectal cancer

Li, Tianhong; Yang, Wancai; Li, Maomi; Byun, Do Sun; Tong, Chang; Nasser, Shannon; Zhuang, Min; Arango, Diego; Mariadason, John M.; Augenlicht, Leonard H.

doi:10.1002/mnfr.200700331

Cited by 79 publications

(126 citation statements)

References 37 publications

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“…SBP1 physically interacts with GPx1 in colonic epithelial cells, and expression of these two Se-containing proteins is regulated reciprocally (21). Expression of SBP1 is frequently downregulated in colorectal carcinoma tissue, and low SBP1 expression levels are correlated with poorer patient survival rates, as shown in two independent studies (43,51). Similar to the selenoproteins SeP and GPx4 (82,81), SBP1 levels increase during enterocytic cellular differentiation.…”

Section: Se-binding Proteinmentioning

confidence: 92%

“…Similar to the selenoproteins SeP and GPx4 (82,81), SBP1 levels increase during enterocytic cellular differentiation. Maximal SBP1 expression is observed in terminally differentiated cells of the intestinal epithelium (51). Knockdown of SBP1 in Caco-2 and SW620 cells was paralleled by a downregulation of the epithelial differentiation marker carcinoembryonic antigen (51).…”

Section: Se-binding Proteinmentioning

confidence: 93%

“…Maximal SBP1 expression is observed in terminally differentiated cells of the intestinal epithelium (51). Knockdown of SBP1 in Caco-2 and SW620 cells was paralleled by a downregulation of the epithelial differentiation marker carcinoembryonic antigen (51). So far, it has not been studied whether SBP1 protein levels in the intestine respond to Se supplementation, which would be a prerequisite for being a candidate mediator of the chemopreventive effects of ingested Se.…”

Section: Se-binding Proteinmentioning

confidence: 99%

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Toward Understanding Success and Failures in the Use of Selenium for Cancer Prevention

Steinbrenner

Speckmann

Sies

2013

Antioxidants & Redox Signaling

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Significance: Adequate and supranutritional selenium (Se) intake, maintaining full expression of selenoproteins, has been assumed to be beneficial for human health with respect to prevention of cancer. Strikingly, the effectiveness of dietary Se supplementation depends on many factors: baseline Se status, age, gender, and genetic background of an individual; type of cancer; and time point of intervention in addition to metabolic conversion and dose of applied Se compounds. Recent Advances: Se intake levels for optimization of plasma selenoproteins in humans have been delineated. Regulation, function, and genetic variants of several selenoproteins have been characterized in the intestine, where Se-mediated prevention of colorectal cancer appears to be particularly promising. Critical Issues: Numerous cell culture and animal studies indicate anticarcinogenic capacity of various Se compounds but, at present, the outcome of human studies is inconsistent and, in large part, disappointing. Moreover, supranutritional Se intake may even trigger adverse health effects, possibly increasing the risk for Type 2 diabetes in Se-replete populations. Future Directions: To improve protocols for the use of Se in cancer prevention, knowledge on cellular and systemic actions of Se compounds needs to be broadened and linked to individual-related determinants such as the occurrence of variants in selenoprotein genes and the Se status. Based on better mechanistic insight, populations and individuals that may benefit most from dietary Se supplementation need to be defined and studied in suitably planned intervention trials.

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Section: Se-binding Proteinmentioning

confidence: 92%

Section: Se-binding Proteinmentioning

confidence: 93%

Section: Se-binding Proteinmentioning

confidence: 99%

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Toward Understanding Success and Failures in the Use of Selenium for Cancer Prevention

Steinbrenner

Speckmann

Sies

2013

Antioxidants & Redox Signaling

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“…Many of these proteins were involved in cellular metabolism while a number were cytoskeletal proteins. Several of these proteins have also been reported to be differentially expressed in either hepatocellular carcinoma or other tumor types, for example alcohol dehydrogenase and aldehyde dehydrogenase [12], carbamyl phosphate synthase [13], selenium binding protein 1 and DNA helicase RuvB-like protein 2 ( [14][15][16]). …”

Section: Proteins Under-expressed In the Tumoral Liver Tissue Comparementioning

confidence: 99%

Proteomic Analysis of Differentially Expressed Proteins in Peripheral Cholangiocarcinoma

Darby

Vuillier-Devillers

Pinault

et al. 2010

Cancer Microenvironment

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Cholangiocarcinoma is an adenocarcinoma of the liver which has increased in incidence over the last thirty years to reach similar levels to other liver cancers. Diagnosis of this disease is usually late and prognosis is poor, therefore it is of great importance to identify novel candidate markers and potential early indicators of this disease as well as molecules that may be potential therapeutic targets. We have used a proteomic approach to identify differentially expressed proteins in peripheral cholangiocarcinoma cases and compared expression with paired non-tumoral liver tissue from the same patients. Two-dimensional fluorescence difference gel electrophoresis after labeling of the proteins with cyanines 3 and 5 was used to identify differentially expressed proteins. Overall, of the approximately 2,400 protein spots visualised in each gel, 172 protein spots showed significant differences in expression level between tumoral and non-tumoral tissue with p<0.01. Of these, 100 spots corresponding to 138 different proteins were identified by mass spectrometry: 70 proteins were over-expressed whereas 68 proteins were under-expressed in tumoral samples compared to nontumoral samples. Among the over-expressed proteins, immunohistochemistry studies confirmed an increased expression of 14-3-3 protein in tumoral cells while α-smooth muscle actin and periostin were shown to be overexpressed in the stromal myofibroblasts surrounding tumoral cells. α-Smooth muscle actin is a marker of myofibroblast differentiation and has been found to be a Ian A. Darby, Karine Vuillier-Devillers, and Émilie Pinault have equally contributed to this work.

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“…The cellular biochemistry of selenium is a complex system that involves the expression of a wide range of selenium-containing proteins (4)(5)(6). Of these proteins, a 56-kDa molecule termed selenium-binding protein 1 (SBP1) was found to be the possible mediator of selenium's anticancer functions (7,8). SBP1 is expressed in various cell types, including liver, heart, and kidney (2), and previous studies have established a solid connection between SBP1 and cancer.…”

Section: Introductionmentioning

confidence: 99%

Decreased Selenium-Binding Protein 1 Enhances Glutathione Peroxidase 1 Activity and Downregulates HIF-1α to Promote Hepatocellular Carcinoma Invasiveness

Huang

Ding

et al. 2012

Clinical Cancer Research

109

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Purpose: We aimed to characterize the role of selenium-binding protein 1 (SBP1) in hepatocellular carcinoma (HCC) invasiveness and underlying clinical significance.Experimental Design: SBP1 expression was measured in stepwise metastatic HCC cell lines by Western blotting. The role of SBP1 in HCC was investigated using siRNA. Immunofluorescence analyses were used to detect the interaction between SBP1 and glutathione peroxidase 1 (GPX1). Nineteen fresh tumor tissues and 323 paraffin-embedded samples were used to validate in vitro findings and to detect the prognostic significance of SBP1, respectively.Results: Inhibition of SBP1 effectively increased cell motility, promoted cell proliferation, and inhibited apoptosis only under oxidative stress; it also greatly enhanced GPX1 activity without altering GPX1 expression and downregulated hypoxia-inducible factor-1a (HIF-1a) expression. SBP1 and GPX1 formed nuclear bodies and colocalized under oxidative stress. In freshly isolated clinical HCC tissues, decreased SBP1 was linked with increased GPX1 activity and correlated with vascular invasion. Tumor tissue microarrays indicated that SBP1 was an independent risk factor for overall survival and disease recurrence; patients with lower SBP1 expression experienced shorter overall survival periods and higher rates of disease recurrence (P < 0.001). Further analyses indicated that the predictive power of SBP1 was more significant for patients beyond the Milan criteria than patients within the Milan criteria.Conclusions: Decreased expression of SBP1 could promote tumor invasiveness by increasing GPX1 activity and diminishing HIF-1a expression in HCC; SBP1 could be a novel biomarker for predicting prognosis and guiding personalized therapeutic strategies, especially in patients with advanced HCC.

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Expression of selenium‐binding protein 1 characterizes intestinal cell maturation and predicts survival for patients with colorectal cancer

Cited by 79 publications

References 37 publications

Toward Understanding Success and Failures in the Use of Selenium for Cancer Prevention

Toward Understanding Success and Failures in the Use of Selenium for Cancer Prevention

Proteomic Analysis of Differentially Expressed Proteins in Peripheral Cholangiocarcinoma

Decreased Selenium-Binding Protein 1 Enhances Glutathione Peroxidase 1 Activity and Downregulates HIF-1α to Promote Hepatocellular Carcinoma Invasiveness

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