Serum Apolipoproteins C-I and C-III Are Reduced in Stomach Cancer Patients: Results from MALDI-Based Peptidome and Immuno-Based Clinical Assays

Cohen, Meital; Yossef, Rami; Erez, Tamar; Kugel, Aleksandra; Welt, Michael; Karpasas, Mark; Bones, Jonathan; Rudd, Pauline M.; Taı̈eb, Julien; Boissin, Herve; Harats, Dror; Noy, Karin; Tekoah, Yoram; Lichtenstein, Rachel G.; Rubin, Eitan; Porgador, Angel

doi:10.1371/journal.pone.0014540

Cited by 46 publications

(35 citation statements)

References 35 publications

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“…Consistent with these findings, APOC1 has been reported to be a promising serum marker for the diagnosis and treatment of multiple cancers, such as gastric cancer,25 pancreatic cancer,26 colorectal cancer,27 thyroid carcinoma,28 and non‐small cell lung cancer 29…”

Section: Discussionsupporting

confidence: 55%

Apolipoprotein C1 promotes prostate cancer cell proliferation in vitro

Sun

Yang

et al. 2018

J Biochem & Molecular Tox

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Here, we aimed to investigate the carcinogenic effects of apolipoprotein C1 (APOC1) in prostate cancer (PCa). APOC1 expression was evaluated in PCa and normal prostate specimens, and lentivirus‐mediated RNA interference was used to knockdown APOC1 in DU145 cells. The effects of APOC1 silencing on cell proliferation, cell cycle arrest, and apoptosis were assessed. APOC1 expression was much higher in PCa tissues than in normal tissues. Moreover, APOC1 silencing inhibited cell proliferation and colony formation, arrested cell cycle progression, and enhanced apoptosis in DU145 cells. Additionally, APOC1 silencing decreased survivin, phospho‐Rb, and p21 levels and increased cleaved caspase‐3 expression. These data supported the procarcinogenic effects of APOC1 in the pathogenesis of PCa and suggested that targeting APOC1 may have applications in the treatment of PCa.

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Section: Discussionsupporting

confidence: 55%

Apolipoprotein C1 promotes prostate cancer cell proliferation in vitro

Sun

Yang

et al. 2018

J Biochem & Molecular Tox

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“…It was also demonstrated to stimulate cell survival signalling pathways and reduce pro-inflammatory cytokine-induced apoptosis [17,18]. Alterations in blood levels of APOC3 were described in several diseases with reduced concentration in liver cirrhosis [19] and cancers [20,21]. Increased levels were also reported [22].…”

Section: Discussionmentioning

confidence: 99%

Identification of serum APOA1 and APOC3 as potential biomarkers of aplastic anemia

Hamzic¹,

Whiting²,

Pettengell³

2016

Clin Med Invest

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Aplastic anemia (AA) is a potentially life threatening bone marrow disorder. The exact mechanisms responsible for AA pathogenesis are unclear and the disease is very difficult to study due to its rarity, heterogeneity in its pathology and limitations in number of cells available for examination. Our aim was to identify serum proteins differentially expressed in untreated AA patients compared to ATG treated patients and healthy controls that might be useful in understanding and monitoring AA. Serum was profiled on CM10 and Q10 ProteinChip arrays using SELDI-TOF/MS, detecting a number of differentially expressed protein peaks. A combined strategy of chromatographic fractionation, 1D gel electrophoresis, passive elution, trypsin digestion and LC-MS/MS analysis, formally identified two discriminatory peaks, further validated with immunodepletion, Western blot and ELISA. They include anti-inflammatory apolipoprotein A1 (APOA1), downregulated in AA compered to controls, and apolipoprotein C3 (APOC3), downregulated in AA compared to both control and ATG treated patients, and represent novel diseaseand therapy-associated AA biomarkers. Inflammatory biomarkers in AA serum support immune-mediated pathology of AA and suppressive action of ATG. Results presented here are the first to describe disease-and therapy-associated proteome changes in these patients. The two identified proteins are, to the best of our knowledge, the first reported serum biomarkers of AA. These biomarkers can potentially be used for disease detection, diagnosis and monitoring and can help in understanding the mechanism of AA. Further studies with additional samples are needed to confirm their importance in the pathogenesis of the disease and their clinical value.

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“…128 Potential biomarkers identified through proteomic analysis of blood include complement component C9 129 and apolipoproteins C-I and C-III. 130 Levels of soluble E-cadherin, hepatocyte growth factor, tissue inhibitor of infection most often produces an immunotolerant phenotype, which is not associated with pathology; disease results from an aggressive Th1 and Th17-biased inflammatory response. 99,100 Still unanswered, however, is the question of why most individuals develop a tolerant phenotype with no disease, while others progress to peptic ulcer or gastric cancer.…”

Section: Proteomicsmentioning

confidence: 99%