Profiling the potential tumor markers of pancreatic ductal adenocarcinoma using 2D-DIGE and MALDI-TOF-MS: Up-regulation of Complement C3 and alpha-2-HS-glycoprotein

Chen, Jiong; Wu, Wen; Chen, Longjiang; Zhou, Hangcheng; Yang, Ren-bao; Hu, Lifen; Zhao, Yue

doi:10.1016/j.pan.2013.03.010

Cited by 33 publications

(23 citation statements)

References 36 publications

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“…The peptide mimicked AHSG, also known as fetuin-A, and we suggest that serum reactivity to fetuin-A shows utility as a sensitive and specific indicator of metastatic disease. Whereas fetuin-A has been implicated as a tumor antigen in several cancer types such as breast cancer (13), glioblastoma (14), and pancreas cancer (15), to our knowledge this report is the first to show involvement of fetuin-A in prostate cancer. We investigated the expression of fetuin-A in a panel of prostate cancer cell lines and observed robust expression of fetuin-A for the highly metastatic PC-3 cells, indicating that expression levels might correlate with metastatic potential as found previously for angiogenic factors (16).…”

Section: Discussionmentioning

confidence: 61%

Discovery and horizontal follow-up of an autoantibody signature in human prostate cancer

Mintz¹,

Rietz

Cardó-Vila

et al. 2015

Proc. Natl. Acad. Sci. U.S.A.

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In response to an urgent need for improved diagnostic and predictive serum biomarkers for management of metastatic prostate cancer, we used phage display fingerprinting to analyze sequentially acquired serum samples from a patient with advancing prostate cancer. We identified a peptide ligand, CTFAGSSC, demonstrating an increased recovery frequency over time. Serum antibody reactivity to this peptide epitope increased in the index patient, in parallel with development of deteriorating symptoms. The antigen mimicking the peptide epitope was identified as alpha-2-HeremansSchmid glycoprotein, also known as fetuin-A. Metastatic prostate cancer cell lines and bone metastasis samples displayed robust fetuin-A expression, and we demonstrated serum immune reactivity to fetuin-A with concomitant development of metastatic castrateresistant disease in a large cohort of prostate cancer patients. Whereas fetuin-A is an established tumor antigen in several types of cancer, including breast cancer, glioblastoma, and pancreas cancer, this report is to our knowledge the first study implicating fetuin-A in prostate cancer and indicating that autoantibodies specific for fetuin-A show utility as a prognostic indicator for prostate cancer patients prone to progress to metastatic disease.cancer biomarker | peptide library | prostate cancer | phage display

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Section: Discussionmentioning

confidence: 61%

Discovery and horizontal follow-up of an autoantibody signature in human prostate cancer

Mintz¹,

Rietz

Cardó-Vila

et al. 2015

Proc. Natl. Acad. Sci. U.S.A.

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“…However presence of the protein is identified in pancreatic ductal adenocarcinoma and hepatocellular carcinoma tissues [26, 27]. AHSG is a 51–67 kDa and belongs to cystatin family of proteins lacking protease-inhibitory capacity [28, 29].…”

Section: Resultsmentioning

confidence: 99%

Proteomic profiling of retinoblastoma by high resolution mass spectrometry

et al. 2016

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BackgroundRetinoblastoma is an ocular neoplastic cancer caused primarily due to the mutation/deletion of RB1 gene. Due to the rarity of the disease very limited information is available on molecular changes in primary retinoblastoma. High throughput analysis of retinoblastoma transcriptome is available however the proteomic landscape of retinoblastoma remains unexplored. In the present study we used high resolution mass spectrometry-based quantitative proteomics to identify proteins associated with pathogenesis of retinoblastoma.MethodsWe used five pooled normal retina and five pooled retinoblastoma tissues to prepare tissue lysates. Equivalent amount of proteins from each group was trypsin digested and labeled with iTRAQ tags. The samples were analyzed on Orbitrap Velos mass spectrometer. We further validated few of the differentially expressed proteins by immunohistochemistry on primary tumors.ResultsWe identified and quantified a total of 3587 proteins in retinoblastoma when compared with normal adult retina. In total, we identified 899 proteins that were differentially expressed in retinoblastoma with a fold change of ≥2 of which 402 proteins were upregulated and 497 were down regulated. Insulin growth factor 2 mRNA binding protein 1 (IGF2BP1), chromogranin A, fetuin A (ASHG), Rac GTPase-activating protein 1 and midkine that were found to be overexpressed in retinoblastoma were further confirmed by immunohistochemistry by staining 15 independent retinoblastoma tissue sections. We further verified the effect of IGF2BP1 on cell proliferation and migration capability of a retinoblastoma cell line using knockdown studies.ConclusionsIn the present study mass spectrometry-based quantitative proteomic approach was applied to identify proteins differentially expressed in retinoblastoma tumor. This study identified the mitochondrial dysfunction and lipid metabolism pathways as the major pathways to be deregulated in retinoblastoma. Further knockdown studies of IGF2BP1 in retinoblastoma cell lines revealed it as a prospective therapeutic target for retinoblastoma.Electronic supplementary materialThe online version of this article (doi:10.1186/s12014-016-9128-7) contains supplementary material, which is available to authorized users.

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“…Several authors describe elevated serum levels of complement components, such as C3, C3c, C5a, and C5b–9/MAC (83–86), as well as soluble iC3b, a complement product generated by the interaction with the abundantly expressed CRegs (87). Complement factor B has been proposed as a promising new serological biomarker for PDAC, supplementing CA 19-9 (88).…”

Section: Potential Role Of Complement In Pancreatic Tumorigenesismentioning

confidence: 99%

Complement in Pancreatic Disease—Perpetrator or Savior?

et al. 2017

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The complement system is a major pillar of the humoral innate immune system. As a first line of defense against pathogens, it mediates early inflammatory response and links different branches of humoral and cellular immunity. Disorders affecting the exocrine pancreas, such as acute pancreatitis, potentially lead to a life-threatening systemic inflammatory response with aberrant activation of complement and coagulation cascades. Pancreatic proteases can activate key effectors of the complement system, which in turn drive local and systemic inflammation. Beyond that, the extent of pancreas–complement interaction covers complex pro- and anti-inflammatory mechanisms, which to this day remain to be fully elucidated. This review provides a comprehensive overview of the pathophysiological role of complement in diseases of the exocrine pancreas, based on existing experimental and clinical data. Participation of complement in acute and chronic pancreatitis is addressed, as well as its role in tumor immunology. Therapeutic strategies targeting complement in these diseases have long been proposed but have not yet arrived in the clinical setting.

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Profiling the potential tumor markers of pancreatic ductal adenocarcinoma using 2D-DIGE and MALDI-TOF-MS: Up-regulation of Complement C3 and alpha-2-HS-glycoprotein

Cited by 33 publications

References 36 publications

Discovery and horizontal follow-up of an autoantibody signature in human prostate cancer

Discovery and horizontal follow-up of an autoantibody signature in human prostate cancer

Proteomic profiling of retinoblastoma by high resolution mass spectrometry

Complement in Pancreatic Disease—Perpetrator or Savior?

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