Differential Protein Expression Profiling by iTRAQ−2DLC−MS/MS of Lung Cancer Cells Undergoing Epithelial-Mesenchymal Transition Reveals a Migratory/Invasive Phenotype

Keshamouni, Venkateshwar G.; Michailidis, George; Grasso, Catherine S.; Anthwal, Shalini; Strahler, John R.; Walker, Angela K.; Reddy, Raju C.; Sudhakar, Akulapalli; Thannickal, Victor J.; Standiford, Theodore J.; Andrews, Philip C.; Omenn, Gilbert S.

doi:10.1021/pr050455t

Cited by 260 publications

(267 citation statements)

References 46 publications

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“…14-3-3 δ is one of the major transforming growth factor-b-induced proteins, which can promote epithelialmesenchymal transition of epithelial cells in cancer cell transformation (Keshamouni et al, 2006). In the present study, the upregulation of 14-3-3 δ was observed in cholangiocarcinoma.…”

Section: Discussionsupporting

confidence: 59%

The Clinicopathological and Prognostic Impact of 14-3-3 Protein Isoforms Expression in Human Cholangiocarcinoma by Immunohistochemistry

Liu²,

Luan³

et al. 2012

Asian Pacific Journal of Cancer Prevention

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The 14-3-3 proteins are highly conserved, ubiquitous molecules involved in a variety of biologic phenomena, such as cell cycle control, and apoptosis. However, their expression in cholangiocarcinoma has not been previously characterized. In this paper, immunohistochemistry using specific anti-14-3-3 monoclonal antibodies was performed on formalin-fixed;, paraffin embedded archival tissue from 86 patients of cholangiocarcinoma. We also examined the correlation between expression and survival rate and clinicopathologic factors such as tumor location, tumor size, pathologic differentiation, lymphatic permeation, lymph node metastasis, and tumor stage. Positive 14-3-3 proteins expression was observed for 6 isoforms (β, σ, γ, θ, δ, η) of these proteins in 86 patients of cholangiocarcinoma. β and σ isoform immunoreactivity was correlated with lymph node metastasis, tumor stage and patients' survival rate. In addition, δ isoform immunoreactivity showed trends with tumor location, tumor size, pathologic differentiation and tumor stage, while the θ isoform was correlated with pathologic differentiation. These results indicated that upregulated expression of some isoforms of 14-3-3 may be a common mechanism for evading apoptosis in cholangiocarcinoma, so that targeting 14-3-3 may be a novel promising strategy for the treatment of this tumor.

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Section: Discussionsupporting

confidence: 59%

The Clinicopathological and Prognostic Impact of 14-3-3 Protein Isoforms Expression in Human Cholangiocarcinoma by Immunohistochemistry

Liu²,

Luan³

et al. 2012

Asian Pacific Journal of Cancer Prevention

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“…Earlier studies have shown that changes beyond 20% from the population mean reported by iTRAQ analysis could be considered significant based on variance and analytical noise analysis (Unwin et al, 2005,in press). Recent work by others (Keshamouni et al, 2006) and our group (Hu et al, in press) also found that ~20% changes observed in iTRAQ data were consistent with the corresponding Western blotting quantification of identical proteins. Quantification accuracy could be affected by many factors, including sample quantity, complexity, analytical hardware limitations, bioinformatic assignment of protein isoforms in addition to biological variations, which we have analyzed extensively (Hu et al, in press).…”

Section: Discussionsupporting

confidence: 82%

A multiplexed proteomics approach to differentiate neurite outgrowth patterns

Liu

D’Mello

Deng

et al. 2006

Journal of Neuroscience Methods

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We report here a method for proteomics pattern discovery by utilizing a self-organizing map approach to analyze data obtained from a novel multiplex iTRAQ ™ proteomics method. Through the application of this technique, we were able to delineate the early molecular events preceding dorsal root ganglia neurite outgrowth induced by either nerve growth factor (NGF) or an immunophilin ligand, JNJ460. Following pattern analysis we discovered that each neurotrophic agent promoted mostly distinct increases in protein expression with few overlapping patterns. In the NGF-treated group, proteins possessing "biosynthesis function" (p < 0.002) and "ribosome localization" (p < 0.0003) were increased, while proteins promoting "organogenesis" (p < 0.004) and related "signal transduction" (p < 0.008) functions were notably increased in the JNJ460-treated group. This study suggests that the properties of neurite outgrowth triggered by NGF and JNJ460 can be distinguished at the proteome level. Multiplexed proteomics analysis, along with pattern discovery bioinformatics tools, has the capability to differentiate subtle neuroproteomics patterns.

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“…Cofilin is overexpressed in the highly invasive C6 rat glioblastoma cell line 72 , A549 human lung cancer cells 73 and human pancreatic cancer cells 74 . The amount of phosphorylated cofilin is decreased in cell lines derived from T-cell lymphoma (Jurkat) and carcinomas from the cervix (HeLa), colon (KM12), liver (HepG2) and kidney (COS1) 75 .…”

Section: The Cofilin Pathway In Tumour Invasionmentioning

confidence: 99%

The cofilin pathway in breast cancer invasion and metastasis

Wang¹,

2007

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Recent evidence indicates that metastatic capacity is an inherent feature of breast tumours and not a rare, late acquired event. This has led to new models of metastasis. The interpretation of expression-profiling data in the context of these new models has identified the cofilin pathway as a major determinant of metastasis. Recent studies indicate that the overall activity of the cofilin pathway, and not that of any single gene within the pathway, determines the invasive and metastatic phenotype of tumour cells. These results predict that inhibitors directed at the output of the cofilin pathway will have therapeutic benefit in combating metastasis.Tumour cell motility is the hallmark of invasion and an essential step in metastasis 1,2 . The identification of molecular pathways that contribute to tumour cell motility and invasion is essential for understanding how motility is initiated in tumour cells and how the tumour microenvironment contributes to cell migration. The identification of the molecular pathways of tumour cell invasion will provide new diagnostic approaches and targets for the treatment of metastatic cancer. Recent studies using new technologies, including highdensity microarray-based expression profiling, intravital imaging and the collection of invasive tumour cells from live tumours, have started to extend the traditional model of metastasis and supply new diagnostic and therapeutic markers of metastatic disease.According to the traditional model of metastasis, metastases result from a process similar to Darwinian evolution whereby natural selection works on individual tumour cells to select © 2007 Nature Publishing Group Correspondence to: J.C. Condeeli@aecom.yu.edu. Competing interests statementThe authors declare no competing financial interests. for stable genetic changes. The cells so selected are very rare, and the metastatic cells that arise from this progressive selection of stable genetic mutations within the primary tumour cause metastasis late in tumour progression 3 . However, studies of mammary tumours in mice [4][5][6][7] , expression profiling of both whole human breast tumours 8,9 and the invasive subpopulation of tumour cells isolated from rat and mouse mammary tumours [10][11][12] suggest that the metastatic ability of breast tumours is encoded throughout the bulk of the primary tumour, involves transient changes in gene expression and is acquired at much earlier stages of tumour progression than postulated by the traditional model. These results suggest that a Darwinian-like evolution is accompanied by, and may contribute to, microenvironmentinduced transient changes in gene expression that support the invasive and metastatic phenotype. These results have led to new models where the microenvironment initiates the expression of genes that induce cell motility, invasion and metastasis 11,13 . In the 'tumour microenvironment invasion model' it is proposed that oncogenic mutations in tumour cells lead to microenvironments that are potentially encoded throughout the b...

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Differential Protein Expression Profiling by iTRAQ−2DLC−MS/MS of Lung Cancer Cells Undergoing Epithelial-Mesenchymal Transition Reveals a Migratory/Invasive Phenotype

Cited by 260 publications

References 46 publications

The Clinicopathological and Prognostic Impact of 14-3-3 Protein Isoforms Expression in Human Cholangiocarcinoma by Immunohistochemistry

The Clinicopathological and Prognostic Impact of 14-3-3 Protein Isoforms Expression in Human Cholangiocarcinoma by Immunohistochemistry

A multiplexed proteomics approach to differentiate neurite outgrowth patterns

The cofilin pathway in breast cancer invasion and metastasis

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