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Dive into the research topics where Olena Masui is active.

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Featured researches published by Olena Masui.


Molecular & Cellular Proteomics | 2013

Quantitative Proteomic Analysis in Metastatic Renal Cell Carcinoma Reveals a Unique Set of Proteins with Potential Prognostic Significance

Olena Masui; Nicole M.A. White; Leroi V. DeSouza; Olga Krakovska; Ajay Matta; Shereen Metias; Bishoy Khalil; Alexander D. Romaschin; R. John Honey; Robert Stewart; Kenneth T. Pace; G. A. Bjarnason; K. W. Michael Siu; George M. Yousef

Metastatic renal cell carcinoma (RCC) is one of the most treatment-resistant malignancies, and patients have a dismal prognosis, with a <10% five-year survival rate. The identification of markers that can predict the potential for metastases will have a great effect in improving patient outcomes. In this study, we used differential proteomics with isobaric tags for relative and absolute quantitation (iTRAQ) labeling and LC-MS/MS analysis to identify proteins that are differentially expressed in metastatic and primary RCC. We identified 1256 non-redundant proteins, and 456 of these were quantified. Further analysis identified 29 proteins that were differentially expressed (12 overexpressed and 17 underexpressed) in metastatic and primary RCC. Dysregulated protein expressions of profilin-1 (Pfn1), 14–3-3 zeta/delta (14–3-3ζ), and galectin-1 (Gal-1) were verified on two independent sets of tissues by means of Western blot and immunohistochemical analysis. Hierarchical clustering analysis showed that the protein expression profile specific for metastatic RCC can distinguish between aggressive and non-aggressive RCC. Pathway analysis showed that dysregulated proteins are involved in cellular processes related to tumor progression and metastasis. Furthermore, preliminary analysis using a small set of tumors showed that increased expression of Pfn1 is associated with poor outcome and is a potential prognostic marker in RCC. In addition, 14–3-3ζ and Gal-1 also showed higher expression in tumors with poor prognosis than in those with good prognosis. Dysregulated proteins in metastatic RCC represent potential prognostic markers for kidney cancer patients, and a greater understanding of their involved biological pathways can serve as the foundation of the development of novel targeted therapies for metastatic RCC.


Molecular & Cellular Proteomics | 2011

Identification of Differentially Regulated Secretome Components During Skeletal Myogenesis

C. Y. X'avia Chan; Olena Masui; Olga Krakovska; Vladimir E. Belozerov; Sébastien N. Voisin; Shaun Ghanny; Jian Chen; Dharsee Moyez; Peihong Zhu; Kennneth R. Evans; John C. McDermott; K. W. Michael Siu

Myogenesis is a well-characterized program of cellular differentiation that is exquisitely sensitive to the extracellular milieu. Systematic characterization of the myogenic secretome (i.e. the ensemble of secreted proteins) is, therefore, warranted for the identification of novel secretome components that regulate both the pluripotency of these progenitor mesenchymal cells, and also their commitment and passage through the differentiation program. Previously, we have successfully identified 26 secreted proteins in the mouse skeletal muscle cell line C2C12 (1). In an effort to attain a more comprehensive picture of the regulation of myogenesis by its extracellular milieu, quantitative profiling employing stable isotope labeling by amino acids in cell culture was implemented in conjunction with two parallel high throughput online reverse phase liquid chromatography-tandem mass spectrometry systems. In summary, 34 secreted proteins were quantified, 30 of which were shown to be differentially expressed during muscle development. Intriguingly, our analysis has revealed several novel up- and down-regulated secretome components that may have critical biological relevance for both the maintenance of pluripotency and the passage of cells through the differentiation program. In particular, the altered regulation of secretome components, including follistatin-like protein-1, osteoglycin, spondin-2, and cytokine-induced apoptosis inhibitor-1, along with constitutively expressed factors, such as fibulin-2, illustrate dynamic changes in the secretome that take place when differentiation to a specific lineage occurs.


Proteomics | 2016

Identification of 14-3-3zeta associated protein networks in oral cancer.

Ajay Matta; Olena Masui; K. W. Michael Siu; Ranju Ralhan

Advancements in genomics, proteomics, and bioinformatics have improved our understanding of gene/protein networks involved in intra‐ and intercellular communication and tumor–host interactions. Using proteomics integrated with bioinformatics, previously we reported overexpression of 14‐3‐3ζ in premalignant oral lesions and oral squamous cell carcinoma tissues in comparison with normal oral epithelium. 14‐3‐3ζ emerged as a novel molecular target for therapeutics and a potential prognostic marker in oral squamous cell carcinoma patients. However, the role of 14‐3‐3ζ in development and progression of oral cancer is not known yet. This study aimed to identify the 14‐3‐3ζ associated protein networks in oral cancer cell lines using IP–MS/MS and bioinformatics. A total of 287 binding partners of 14‐3‐3ζ were identified in metastatic (MDA1986) and nonmetastatic (SCC4) oral cancer cell lines including other 14‐3‐3 isoforms (2%), proteins involved in apoptosis (2%), cytoskeleton (9%), metabolism (16%), and maintenance of redox potential (2%). Our bioinformatics analysis revealed involvement of 14‐3‐3ζ in protein networks regulating cell cycle, proliferation, apoptosis, cellular trafficking, and endocytosis in oral cancer. In conclusion, our data revealed several novel protein interaction networks involving 14‐3‐3ζ in oral cancer progression and metastasis.


Journal of Clinical Oncology | 2013

Relative quantification of protein expression in metastatic renal cell carcinoma using iTRAQ LC-MS/MS analysis reveals galectin-1 as a potential prognostic marker and therapeutic target.

Nicole M.A. White; Olena Masui; Leroi V. DeSouza; Olga Krakovska; Ajay Matta; Georg A. Bjarnason; K. W. Michael Siu; George M. Yousef

412 Background: Metastatic renal cell carcinoma (RCC) is one of the most treatment-resistant cancers. Identification of proteins involved in tumor progression will help gain a better understanding of the disease and will form the basis for the identification of novel therapeutic targets. METHODS Using six fresh-frozen primary and six unmatched metastatic RCC tumors, we used iTRAQ labeling and LC-MS/MS analysis to identify proteins differentially expressed in metastatic versus primary RCC. We verified protein expression by western blot and immunohistochemical analyses and the measured the effect of dysregulated protein expression on biological processes with RCC cell line models. RESULTS After analysis, we identified 29 proteins differentially expressed in metastatic versus primary RCC. We verified expressions of profilin-1, 14-3-3 zeta/delta, and galectin-1 (Gal-1) on two independent tissue sets by western blot (10 primary and 10 metastatic RCC tissues) and immunohistochemistry (22 primary and 23 metastatic tissues). Overexpression of Gal-1 in CAKI-1 cells lead to decreased actin, increased vimentin expression, and increased cellular migration. Additionally, when Gal-1 was decreased via siRNA, cells showed decreased cellular migration. Protein array analysis showed expression of cell motility-related proteins HSP27, JNK, and RSK, were altered after siRNA transfection. We also showed that Gal-1 expression was increased in response to HIF-1alpha. Furthermore, we analyzed the expression of Gal-1 mRNA in 404 RCC patients using the Cancer Genome Anatomy Project, and found that patients who had higher Gal-1 expression in the primary RCC had significantly decreased overall survival (41 vs. 78 months; p < 0.01). CONCLUSIONS Gal-1 is increased in metastatic RCC and can effect cell migration by targeting proteins involved in cell motility. This may be a downstream effect of HIF-1α dysregulation. Decreased Gal-1 significantly decreased cellular migration suggesting Gal-1 may serve as a potential therapeutic target. Additionally, we showed that increased Gal-1 expression was associated with decreased overall survival.


Proteomics | 2011

Identification of proteins secreted by head and neck cancer cell lines using LC‐MS/MS: Strategy for discovery of candidate serological biomarkers

Ranju Ralhan; Olena Masui; Leroi V. DeSouza; Ajay Matta; Muzafar A. Macha; K. W. Michael Siu


Oncotarget | 2014

Quantitative proteomic analysis reveals potential diagnostic markers and pathways involved in pathogenesis of renal cell carcinoma

Nicole M.A. White; Olena Masui; Leroi V. DeSouza; Olga Krakovska; Shereen Metias; Alexander D. Romaschin; R. John D'a. Honey; Robert Stewart; Kenneth T. Pace; Jason S. Lee; Michael A.S. Jewett; Georg A. Bjarnason; K. W. Michael Siu; George M. Yousef


Journal of Proteome Research | 2010

Secretome-based identification and characterization of potential biomarkers in thyroid cancer.

Lawrence Kashat; Anthony K.-C. So; Olena Masui; X. Simon Wang; Jun Cao; Xianwang Meng; Christina MacMillan; Laurie E. Ailles; K. W. Michael Siu; Ranju Ralhan; Paul G. Walfish


Tumor Biology | 2014

Identification and validation of dysregulated metabolic pathways in metastatic renal cell carcinoma

Nicole M.A. White; Daniel W. Newsted; Olena Masui; Alexander D. Romaschin; K. W. Michael Siu; George M. Yousef


Journal of Translational Medicine | 2015

Nuclear heterogeneous nuclear ribonucleoprotein D is associated with poor prognosis and interactome analysis reveals its novel binding partners in oral cancer

Manish Kumar; Ajay Matta; Olena Masui; Gunjan Srivastava; Jatinder Kaur; Alok Thakar; Nootan Kumar Shukla; Ajoy Roychoudhury; Meherchand Sharma; Paul G. Walfish; K. W. Michael Siu; Shyam S. Chauhan; Ranju Ralhan


Clinical & Experimental Metastasis | 2015

Alpha-enolase is a potential prognostic marker in clear cell renal cell carcinoma

Nicole White-Al Habeeb; Ashley Di Meo; Andreas Scorilas; Fabio Rotondo; Olena Masui; Annetta Seivwright; Manal Gabril; Andrew Girgis; Michael A.S. Jewett; George M. Yousef

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