Detection and identification of peroxiredoxin 3 as a biomarker in hepatocellular carcinoma by a proteomic approach

Qiao, Bingbing; Wang, Jiajia; Xie, Jianfei; Niu, Ying; Ye, Shaojun; Wan, Qiquan; Ye, Qifa

doi:10.3892/ijmm.2012.916

Cited by 22 publications

(12 citation statements)

References 24 publications

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“…PRX3 is consistently up-regulated in prostate cancers [55], is over-expressed in greater than 90% of hepatocellular carcinomas [56], and increases in abundance during malignant progression of cervical cancer [57]. Inhibition of PRX3 expression in breast cancer cells induces cell cycle arrest and impairs cell proliferation [58].…”

Section: Discussionmentioning

confidence: 99%

Peroxiredoxin 3 Is a Redox-Dependent Target of Thiostrepton in Malignant Mesothelioma Cells

et al. 2012

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Thiostrepton (TS) is a thiazole antibiotic that inhibits expression of FOXM1, an oncogenic transcription factor required for cell cycle progression and resistance to oncogene-induced oxidative stress. The mechanism of action of TS is unclear and strategies that enhance TS activity will improve its therapeutic potential. Analysis of human tumor specimens showed FOXM1 is broadly expressed in malignant mesothelioma (MM), an intractable tumor associated with asbestos exposure. The mechanism of action of TS was investigated in a cell culture model of human MM. As for other tumor cell types, TS inhibited expression of FOXM1 in MM cells in a dose-dependent manner. Suppression of FOXM1 expression and coincidental activation of ERK1/2 by TS were abrogated by pre-incubation of cells with the antioxidant N-acetyl-L-cysteine (NAC), indicating its mechanism of action in MM cells is redox-dependent. Examination of the mitochondrial thioredoxin reductase 2 (TR2)-thioredoxin 2 (TRX2)-peroxiredoxin 3 (PRX3) antioxidant network revealed that TS modifies the electrophoretic mobility of PRX3. Incubation of recombinant human PRX3 with TS in vitro also resulted in PRX3 with altered electrophoretic mobility. The cellular and recombinant species of modified PRX3 were resistant to dithiothreitol and SDS and suppressed by NAC, indicating that TS covalently adducts cysteine residues in PRX3. Reduction of endogenous mitochondrial TRX2 levels by the cationic triphenylmethane gentian violet (GV) promoted modification of PRX3 by TS and significantly enhanced its cytotoxic activity. Our results indicate TS covalently adducts PRX3, thereby disabling a major mitochondrial antioxidant network that counters chronic mitochondrial oxidative stress. Redox-active compounds like GV that modify the TR2/TRX2 network may significantly enhance the efficacy of TS, thereby providing a combinatorial approach for exploiting redox-dependent perturbations in mitochondrial function as a therapeutic approach in mesothelioma.

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Section: Discussionmentioning

confidence: 99%

Peroxiredoxin 3 Is a Redox-Dependent Target of Thiostrepton in Malignant Mesothelioma Cells

et al. 2012

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“…By utilizing more sensitive machines and methods, low abundance proteins that change with cancer development can be found and may be more directly related to the cancer. Using such methods, proteins such as peroxiredoxin 3 (Ai et al, 2006; Chen et al, 2010b; Guo et al, 2007; Li et al, 2008; Lu et al, 2010; Qiao et al, 2012; Song et al, 2009; Wang, 2007; Yue et al, 2007) and osteopontin have been identified as potential markers of HCC (Abu El Makarem et al, 2011; Chen et al, 2010a; Chen et al, 2011; Kim et al, 2006; Lin et al, 2011; Phillips et al, 2012; Qin and Tang, 2004; Shang et al, 2012; Tang et al, 2004; Ye et al, 2003; Zekri et al, 2011). While these markers have been shown to be elevated in other cancers, they may still have great value in the early detection of liver cancer (Chahed et al, 2008; Lehtonen et al, 2004; McAllister et al, 2008; Mirza et al, 2008; Park et al, 2008; Park et al, 2007; Reiniger et al, 2007; Schremmer et al, 2007; Tigrani and Weydert, 2007; Tuck et al, 2007; Whiteaker et al, 2007).…”

Section: Proteomic Identification Of Biomarkers Of Liver Cancermentioning

confidence: 99%

Glycosylation and Liver Cancer

Mehta

Herrera

Block

2015

Advances in Cancer Research

120

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Liver cancer is the 5th most common cancer, but the 2nd leading cause of cancer death, in the world, with more than 700,000 fatalities annually. The major etiology of liver cancer is infection with an hepatotropic virus such as hepatitis B virus (HBV) or hepatitis C virus infection (HCV). While chronic viral infection remains the main cause of liver disease and risk of HCC, rates of non –viral associated HCC are occurring at an alarmingly increasing rate. Like many cancers, survival rates are closely associated with time of detection. If HCC is caught early, survival rates can be as high as 50%. Regrettably, most cases of HCC are caught late where survival rates can be as low as 2–7%. Thus, there has been great interest in discovering serum biomarkers that could be used to identify those with HCC. To this end, many groups have examined the N-linked glycans to identify changes that occur with HCC. As the liver secretes the vast majority of proteins into the serum, this has often been a starting point for study. In serum, alterations in core fucosylation, outer-arm fucosylation, increased sialylation and glycan branching have been observed in patients with HCC. Similar findings have been found directly in HCC tissue suggesting that these glycan changes may play a role in tumor formation and development.

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“…Numerous genomic and proteomic screening studies have been employed to identify potential biomarkers of HCC[18-24] but to date the markers identified in these studies have not been clinically fruitful. Because the liver is the hub of carbohydrate, amino acid, and lipid metabolism[25,26], chronic liver diseases undoubtedly disrupt normal metabolic function.…”

Section: Introductionmentioning

confidence: 99%

Disease monitoring of hepatocellular carcinoma through metabolomics

Fitian

Cabrera

2017

WJH

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We elucidate major pathways of hepatocarcinogenesis and accurate diagnostic metabolomic biomarkers of hepatocellular carcinoma (HCC) identified by contemporary HCC metabolomics studies, and delineate a model HCC metabolomics study design. A literature search was carried out on Pubmed for HCC metabolomics articles published in English. All relevant articles were accessed in full text. Major search terms included “HCC”, “metabolomics”, “metabolomics”, “metabonomic” and “biomarkers”. We extracted clinical and demographic data on all patients and consolidated the lead candidate biomarkers, pathways, and diagnostic performance of metabolomic expression patterns reported by all studies in tables. Where reported, we also extracted and summarized the metabolites and pathways most highly associated with the development of cirrhosis in table format. Pathways of lysophospholipid, sphingolipid, bile acid, amino acid, and reactive oxygen species metabolism were most consistently associated with HCC in the cited works. Several studies also elucidate metabolic alterations strongly associated with cirrhosis, with γ-glutamyl peptides, bile acids, and dicarboxylic acids exhibiting the highest capacity for stratifying cirrhosis patients from appropriately matched controls. Collectively, global metabolomic profiles of the referenced works exhibit a promising diagnostic capacity for HCC at a capacity greater than that of conventional diagnostic biomarker alpha-fetoprotein. Metabolomics is a powerful strategy for identifying global metabolic signatures that exhibit potential to be leveraged toward the screening, diagnosis, and management of HCC. A streamlined study design and patient matching methodology may improve concordance among metabolomic datasets in future works.

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Detection and identification of peroxiredoxin 3 as a biomarker in hepatocellular carcinoma by a proteomic approach

Cited by 22 publications

References 24 publications

Peroxiredoxin 3 Is a Redox-Dependent Target of Thiostrepton in Malignant Mesothelioma Cells

Peroxiredoxin 3 Is a Redox-Dependent Target of Thiostrepton in Malignant Mesothelioma Cells

Glycosylation and Liver Cancer

Disease monitoring of hepatocellular carcinoma through metabolomics

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