A1BG and C3 are overexpressed in patients with cervical intraepithelial neoplasia III

Canales, Norma Angélica Galicia; Marina, Vicente Madrid; Castro, Jorge Salmerón; Jiménez, Alfredo Antúnez; Mendoza‐Hernández, Guillermo; Langley, Elizabeth; Roman, Margarita Bahena; Castro-Romero, Julieta Ivone

doi:10.3892/ol.2014.2195

Cited by 20 publications

(13 citation statements)

References 52 publications

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“…We found that alpha-1-B-glycoprotein (A1BG) and T4 surface glycoprotein precursor (TSGP) were both up-regulated in DEW and SP, and the expression was over two-fold higher in SP than DEW (Figure 1; Table 1). A1BG was reportedly involved in a number of diseases such as endometrial cancer, cervical cancer and cervical squamous cell carcinoma (30), and was also elevated in hepatic fibrosis patients, which allowed such patients to be easily distinguished from HI (31). TSGP was associated with T-cell costimulation, positive regulation of interleukin-2 biosynthesis, T-cell receptor complex formation, extracellular matrix structural constituents, the transmembrane receptor protein tyrosine kinase signaling pathway, early endosomes, innate immune responses, and proteinaceous extracellular matrix and MHC class II protein complexes.…”

Section: Glycoproteinsmentioning

confidence: 99%

Proteomic profiling change during the early development of silicosis disease

Miao¹,

Ding²,

Xin³

et al. 2016

J. Thorac. Dis.

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Background: Silicosis is one of several severe occupational diseases for which effective diagnostic tools during early development are currently unavailable. In this study we focused on proteomic profiling during the early stages of silicosis to investigate the pathophysiology and identify the proteins involved.Methods: Two-dimensional (2D) gel electrophoresis and MALDI-TOF-MS were used to assess the proteomic differences between healthy individuals (HI), dust-exposed workers without silicosis (DEW) and silicosis patients (SP). Proteins abundances that differed by a factor of two-fold or greater were subjected to more detailed analysis, and enzyme linked to immunosorbent assay (ELISA) was employed to correlate with protein expression data.Results: Compared with HI, 42 proteins were more abundant and 8 were less abundant in DEW, and these were also differentially accumulated in SP. Closer inspection revealed that serine protease granzyme A, alpha-1-B-glycoprotein (A1BG) and the T4 surface glycoprotein precursor (TSGP) were among the up-regulated proteins in DEW and SP. Significant changes in serine proteases, glycoproteins and protooncogenes may be associated with the response to cytotoxicity and infectious pathogens by activation of T cells, positive regulation of extracellular matrix structural constituents and immune response, and fibroblast proliferation. Up-regulation of cytokines included TNFs, interferon beta precursor, interleukin 6, atypical chemokine receptor 2, TNFR13BV, and mutant IL-17F may be involved in the increased and persistent immune response and fibrosis that occurred during silicosis development.Conclusions: Granzymes, glycoproteins, cytokines and immune factors were dramatically involved in the immune response, metabolism, signal regulation and fibrosis during the early development of silicosis.Proteomic profiling has expanded our understanding of the pathogenesis of silicosis, and identified a number of targets that may be potential biomarkers for early diagnosis of this debilitating disease. J Thorac Dis 2016;8(3):329-341 jtd.amegroups.com extracellular apoptosis related factor (ECM), cytokines and lipid-associated proteins were all reportedly involved in the development of silicosis (3,4). Unfortunately, an effective method involving biomarkers for early diagnosis remained unavailable at present.Significant cellular and molecular alterations ensued following inhalation and deposition of silica minerals in lung tissues (5). Lower-level exposure to silica particles triggered reversible inflammatory lesions, whereas highlevel exposure led to long-term effects on inflammation, cell proliferation, deposition of collagen and extracellular matrix components in mesenchymal cells (1). Alveolar macrophages (AM), neutrophils, T-lymphocytes and mast cells were all involved in fibrogenesis, and cross-talk between these cells played an important role in disease progression. In studies on the interaction of mast cells and neutrophils in mice, animals with intact mast cells endured more severe lung lesi...

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Section: Glycoproteinsmentioning

confidence: 99%

Proteomic profiling change during the early development of silicosis disease

Miao¹,

Ding²,

Xin³

et al. 2016

J. Thorac. Dis.

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“…The blots were washed three times with TBST and an enhanced chemiluminescence system (ImageQuant LAS 4000 mini; GE Healthcare Japan, Tokyo, Japan) was used to detect the bands. The band densities of PARP and Bcl-xL were measured with ImageJ (National Institutes of Health, Bethesda, MD, USA), and densitometry analysis was performed as previously described ( 24 ).…”

Section: Methodsmentioning

confidence: 99%

Suppression of STAT5b in pancreatic cancer cells leads to attenuated gemcitabine chemoresistance, adhesion and invasion

et al. 2016

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Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal solid malignancies, and there is an urgent need for new therapeutic strategies based on the molecular biology of PDAC. Signal transducers and activators of transcription 5 (STAT5) are known to be activated in a variety of malignancies and involved in tumor proliferation, apoptosis, and invasion, whereas the expression and biological role of STAT5b in PDAC are less clearly defined. In the present study, we examined the expression and role of STAT5b in human pancreatic cancer cell lines. Expressions of STAT5b mRNA and protein were detected in eight kinds of pancreatic cancer cells. Confocal microscopy and western blot analysis indicated that STAT5b is localized in both cytoplasm and nuclei. Immunoprecipitation analysis revealed tyrosine phosphorylation of STAT5b in pancreatic cancer cells. These results indicate that STAT5b in pancreatic cancer cells is constitutively activated. STAT5b shRNA clones in PANC-1 cells, which express relatively high levels of STAT5b, exhibited reduced chemoresistance against gemcitabine, adhesion and invasion compared to sham. On the other hand, AsPC-1 and BxPC3 cells, which express relatively low levels of STAT5b, exhibited reduced chemoresistance compared to PANC-1 cells. Moreover, STAT5b overexpression clones in AsPC-1 cells exhibited increased chemoresistance compared to sham. STAT5b shRNA clones in PANC-1 cells were more sensitive to the proapoptotic actions of gemcitabine, as evidenced by PARP and cleaved caspase-3 activation. Gemcitabine also significantly reduced Bcl-xL levels in the STAT5b shRNA-expressing cells. We also investigated the clinicopathological characteristics of STAT5b expression of PDAC. Although a significant correlation between STAT5b expression and overall survival rates was not observed, a significant correlation with main pancreatic duct invasion was observed. These findings suggest that STAT5b confers gemcitabine chemoresistance and promotes cell adherence and invasiveness in pancreatic cancer cells. Targeting STAT5b may lead to novel therapeutic strategies for PDAC.

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“…Functional annotation of A1BG is yet poorly understood, although it is overexpressed in several types of cancer, including CRC [56,57], and is ubiquitously expressed in many tissues under normal conditions. While studying CRC, A1BG has been observed to be abundant vesicles, suggesting its role in modulation of the immune response during cancer development [58]. The A1BG protein shows significant homology with immunoglobulin family proteins.…”

Section: Repercussion Of Proteins With Widely Proposed and Yet To Be mentioning

confidence: 99%

Revelation of Proteomic Indicators for Colorectal Cancer in Initial Stages of Development

et al. 2020

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Background: Colorectal cancer (CRC) at a current clinical level is still hardly diagnosed, especially with regard to nascent tumors, which are typically asymptotic. Searching for reliable biomarkers of early diagnosis is an extremely essential task. Identification of specific post-translational modifications (PTM) may also significantly improve net benefits and tailor the process of CRC recognition. We examined depleted plasma samples obtained from 41 healthy volunteers and 28 patients with CRC at different stages to conduct comparative proteome-scaled analysis. The main goal of the study was to establish a constellation of protein markers in combination with their PTMs and semi-quantitative ratios that may support and realize the distinction of CRC until the disease has a poor clinical manifestation. Results: Proteomic analysis revealed 119 and 166 proteins for patients in stages I–II and III–IV, correspondingly. Plenty of proteins (44 proteins) reflected conditions of the immune response, lipid metabolism, and response to stress, but only a small portion of them were significant (p < 0.01) for distinguishing stages I–II of CRC. Among them, some cytokines (Clusterin (CLU), C4b-binding protein (C4BP), and CD59 glycoprotein (CD59), etc.) were the most prominent and the lectin pathway was specifically enhanced in patients with CRC. Significant alterations in Inter-alpha-trypsin inhibitor heavy chains (ITIH1, ITIH2, ITIH3, and ITIH4) levels were also observed due to their implication in tumor growth and the malignancy process. Other markers (Alpha-1-acid glycoprotein 2 (ORM2), Alpha-1B-glycoprotein (A1BG), Haptoglobin (HP), and Leucine-rich alpha-2-glycoprotein (LRG1), etc.) were found to create an ambiguous core involved in cancer development but also to exactly promote tumor progression in the early stages. Additionally, we identified post-translational modifications, which according to the literature are associated with the development of colorectal cancer, including kininogen 1 protein (T327-p), alpha-2-HS-glycoprotein (S138-p) and newly identified PTMs, i.e., vitamin D-binding protein (K75-ac and K370-ac) and plasma protease C1 inhibitor (Y294-p), which may also contribute and negatively impact on CRC progression. Conclusions: The contribution of cytokines and proteins of the extracellular matrix is the most significant factor in CRC development in the early stages. This can be concluded since tumor growth is tightly associated with chronic aseptic inflammation and concatenated malignancy related to loss of extracellular matrix stability. Due attention should be paid to Apolipoprotein E (APOE), Apolipoprotein C1 (APOC1), and Apolipoprotein B-100 (APOB) because of their impact on the malfunction of DNA repair and their capability to regulate mTOR and PI3K pathways. The contribution of the observed PTMs is still equivocal, but a significant decrease in the likelihood between modified and native proteins was not detected confidently.

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A1BG and C3 are overexpressed in patients with cervical intraepithelial neoplasia III

Cited by 20 publications

References 52 publications

Proteomic profiling change during the early development of silicosis disease

Proteomic profiling change during the early development of silicosis disease

Suppression of STAT5b in pancreatic cancer cells leads to attenuated gemcitabine chemoresistance, adhesion and invasion

Revelation of Proteomic Indicators for Colorectal Cancer in Initial Stages of Development

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