Proteomics-based identification of a group of apoptosis-related proteins and biomarkers in gastric cancer

Bai, Zhigang; Ye, Yingjiang; Liang, Bin; Xu, Feng; Zhang, Hui; Zhang, Yanbin; Peng, Jiarou; Shen, Danhua; Cui, Zhirong; Zhang, Zhongtao; Wang, Shan

doi:10.3892/ijo.2010.873

Cited by 42 publications

(37 citation statements)

References 37 publications

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“…1 ENO1 has been considered to be a diagnostic marker for many kind of tumors, 9,14,36,37 and overexpression of ENO1 is a common scenario in several cancers and is closely connected with tumor progression and poor clinical out-comes. 10,13,38 As ENO1 has an important role in tumorigenesis and tumor development, it will be important to further characterize the mechanisms through which ENO1 is regulated. Many reports have demonstrated that ENO1 can be regulated at different levels by multiple factors.…”

Section: Discussionmentioning

confidence: 99%

“…2-D electrophoresis was performed using Bergman’s method as previously described. 13 Following 2-D electrophoresis, gels were scanned into a computer. The 2-D gel profile was analyzed using the PDQuest software (Bio-Rad).…”

Section: Methodsmentioning

confidence: 99%

“…1,3–5 Remarkably, accumulating evidence suggests that ENO1 can function as an oncogenic protein by promoting cell proliferation, invasion and metastasis. ENO1 expression is frequently increased in diverse tumors, including head and neck, 6 thyroid, 7 breast, 8 lung, 9,10 prostate, 11 colon and gastric cancer, 12,13 glioma 14 and cholangiocarcinoma. 15 Moreover, overexpression of ENO1 is positively associated with progression and poor prognosis in several tumors.…”

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confidence: 99%

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FBXW7 negatively regulates ENO1 expression and function in colorectal cancer

Zhan

Wang

Zhao

et al. 2015

Laboratory Investigation

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FBXW7 (F-box and WD40 domain protein 7) is a tumor suppressor frequently inactivated in human cancers. The precise molecular mechanisms by which FBXW7 exerts antitumor activity remain under intensive investigation and are thought to relate in part to FBXW7-mediated destruction of key cancer-relevant proteins. Enolase 1 (ENO1) possesses oncogenic activity and is often overexpressed in various human cancers, besides its critical role in glycolysis. However, the detailed regulatory mechanisms of ENO1 expression remain unclear. Here we show that the elevated expression of ENO1 was identified in FBXW7-depletion HCT116 cells through two-dimensional protein electrophoresis and mass spectrometry assays (2DE-MS). Subsequent western blotting and immunohistochemical assays confirmed that ENO1 expression reversely correlates with FBXW7 expression in several cells and colon cancer tissues. Furthermore, we show that FBXW7 physically binds to ENO1 and targets ENO1 for ubiquitin-mediated degradation. Functionally, we found that FBXW7 suppresses the ENO1-induced gene expression, lactate production, cell proliferation and migration. These findings suggest that ENO1 is a novel substrate of FBXW7, and its activity can be negatively regulated by FBXW7 at the posttranslational level. Our work provides a novel molecular insight into FBXW7-directed tumor suppression through regulation of ENO1.

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Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

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confidence: 99%

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FBXW7 negatively regulates ENO1 expression and function in colorectal cancer

Zhan

Wang

Zhao

et al. 2015

Laboratory Investigation

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“…After challenging PBMCs with PWM for ten days, cells were lysed and Grp94 detected in WB. To exclude that stimulation with the mitogen could induce an increase in the expression of other HSPs also identified as tumor antigens [15, 33] we measured the expression of both HSP90 and Grp78 in cell lysates. As shown in Figure 2 (panel C), incubation with PWM led to a marked rise in the Grp94 expression that, at variance with what occurred in the corresponding un-stimulated control in which Grp94 appeared at its expected molecular mass (100 kDa for the monomer, and 200 kDa for the dimer in non-reducing conditions), was found at higher molecular masses testifying the formation of big complexes (Figure 2C).…”

Section: Resultsmentioning

confidence: 99%

Grp94 in complexes with IgG is a soluble diagnostic marker of gastrointestinal tumors and displays immune-stimulating activity on peripheral blood immune cells

et al. 2016

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Glucose-regulated protein94 (Grp94), the most represented endoplasmic reticulum (ER)-resident heat shock protein (HSP), is a tumor antigen shared by different types of solid and hematological tumors. The tumor-specific feature of Grp94 is its translocation from the ER to the cell surface where it displays pro-oncogenic functions. This un-physiological location has important implications for both the tumor pathology and anti-tumor therapy. We wanted to address the question of whether Grp94 could be measured as liquid marker in cancer patients in order to make predictions of diagnostic and therapeutic relevance for the tumor. To this aim, we performed an in-depth investigation on patients with primary tumors of the gastrointestinal (GI) tract, using different methodological approaches to detect Grp94 in tumor tissues, plasma and peripheral blood mononuclear cells (PBMCs). Results indicate that Grp94 is not only the antigen highly expressed in any tumor tissue and in cells of tumor infiltrates, mostly B lymphocytes, but it is also found in the circulation. However, the only form in which Grp94 was detected in the plasma of any patients and in B lymphocytes induced to proliferate, was that of stable complexes with Immunoglobulin (Ig)G. Using a specific immune-enzyme assay to measure plasma Grp94-IgG complexes, we showed that Grp94-IgG complexes were significantly increased in cancer patients compared to healthy control subjects, serving as diagnostic tumor biomarker. Results also demonstrate that the stimulation of patient PBMCs with Grp94-IgG complexes led to an increased secretion of inflammatory cytokines that might drive a potentially beneficial anti-tumor effect.

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“…Wang et al [22] discovered that Rab GDIβ was significantly up-regulated in the highly metastatic gallbladder carcinoma cells GBC-SD18H compared with the poorly metastatic GBC-SD18L cell line. Proteomic analysis results have also shown that Rab GDIβ expressions in gastric cancer [23] and ovarian cancer [24] were aberrant compared with those in normal tissues. Therefore, Rab GDIβ possibly participates in cancer initiation and progression.…”

Section: Introductionmentioning

confidence: 99%

Bioinformatics analysis of Rab GDP dissociation inhibitor beta and its expression in non-small cell lung cancer

Zhou

Guo²,

Jiang

et al. 2014

Diagn Pathol

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BackgroundLung cancer has been considered as one of the most important causes of cancer-related mortality worldwide. To predict lung cancer, researchers identified several molecular markers. However, many underlying markers of lung cancer remain unclear. One of these markers is Rab GDP dissociation inhibitor beta (GDIβ), which is related to tumorigenicity, development and invasion. This study was designed to analyze the biological characteristics of Rab GDIβ and to detect the mRNA and protein expressions of Rab GDIβ in lung cancer cells; this study also aimed to investigate the functions of this protein in lung cancer.MethodUsing online software from the websites of NCBI, ProtParam and so on, we analyzed the biological characteristics of Rab GDIβ. RT-PCR was performed to detect gene expressions in A549 and 16HBE cell lines and immunohistochemistry (IHC) staining was conducted to detect Rab GDIβ protein expression in 57 cases of human lung cancer tissues and 19 cases of normal lung tissues. The association of protein expression with patient clinical and pathological characteristics was assessed in each dataset.ResultsBioinformatic analysis on Rab GDIβ: The mRNA of human Rab GDIβ contains two transcript variants; the common structural elements of the two proteins are mainly α-helix, random coil, β-turn and extended strand. Three and four transmembrane domains could be found in the entire polypeptide chain of protein variants 1 and 2, respectively; both transcript variants are hydrophilic and soluble proteins. The RT-PCR result: The mRNA expression of Rab GDIβ was down-regulation in A549 cells compared with that in 16HBE cells. The IHC result: The protein expression of Rab GDIβ in lung cancer cells was significantly lower than that in normal lung tissues (P <0.05) but was not correlated with patients’ age, gender, tumor size, pathological type, differentiation, lymph node metastasis, distant metastasis and TNM stage.ConclusionThe expression of Rab GDIβ was low in non-small cell lung cancer (NSCLC). Hence, Rab GDIβ may be a tumor suppressor and could function as an indicator of tumorigenesis in NSCLC; nevertheless, this result should be further studied.Virtual SlidesThe virtual slide(s) for this article can be found here: http://www.diagnosticpathology.diagnomx.eu/vs/13000_2014_201

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Proteomics-based identification of a group of apoptosis-related proteins and biomarkers in gastric cancer

Cited by 42 publications

References 37 publications

FBXW7 negatively regulates ENO1 expression and function in colorectal cancer

FBXW7 negatively regulates ENO1 expression and function in colorectal cancer

Grp94 in complexes with IgG is a soluble diagnostic marker of gastrointestinal tumors and displays immune-stimulating activity on peripheral blood immune cells

Bioinformatics analysis of Rab GDP dissociation inhibitor beta and its expression in non-small cell lung cancer

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