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Loss of disabled-2 expression is an early event in esophageal squamous tumorigenesis

World Journal of Gastroenterology 2006年第37期12卷 6041-6045页

作者： Kumar Anupam Chatopadhyay Tusharkant Siddhartha Datta Gupta ralhan ranju Department of Biochemistry All India Institute of Medical Sciences Ansari Nagar New Delhi 110029 India Department of GI Surgery All India Institute of Medical Sciences Ansari Nagar New Delhi 110029 India Department of Pathology All India Institute of Medical Sciences Ansari Nagar New Delhi 110029 India

AIM: Disabled-2 (DAB2) is a candidate tumor-suppressor gene identified in ovarian cancer that negatively influences mitogenic signal transduction of growth factors and blocks ras activity. In a recent study, we observed down-regulation of DAB2 transcripts in ESCCs using cDNA microarrays. In the present study, we aimed to determine the clinical significance of loss of DAB2 protein in esophageal tumorigenesis, hypothesizing that DAB2 promoter hypermethylation-mediated gene silencing may account for loss of the protein. METHODS: DAB2 expression was analyzed by immunohistochemistry in 50 primary esophageal squamous cell carcinomas (ESCCs), 30 distinct hyperplasia, 15 dysplasia and 10 non-malignant esophageal tissues. To determine whether promoter hypermethylation contributes to loss of DAB2 expression in ESCCs, methylation status of DAB2 promoter was analyzed in DAB2 immuno-negative tumors using methylation-specifi c PCR. RESULTS: Loss of DAB2 protein was observed in 5/30 (17%) hyperplasia, 10/15 (67%) dysplasia and 34/50 (68%) ESCCs. Significant loss of DAB2 protein was observed from esophageal normal mucosa to hyperplasia, dysplasia and invasive cancer (Ptrend < 0.001). Promoter hypermethylation of DAB2 was observed in 2 of 10 (20%) DAB2 immuno-negative ESCCs. CONCLUSION: Loss of DAB2 protein expression occurs in early pre-neoplastic stages of development of esophageal cancer and is sustained down the tumorigenic pathway. Infrequent DAB2 promoter methylation in ESCCs suggests that epigenetic genesilencing is only one of the mechanisms causing loss of DAB2 expression in ESCCs.

关键词： Disabled-2 DOC-2 Esophageal cancer Promoter hypermethylation Dysplasia

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siRNA-mediated downregulation of TC21 sensitizes esophageal cancer cells to cisplatin

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World Journal of Gastroenterology 2012年第31期18卷 4127-4135页

作者： Md.Raghibul Hasan Shyam Singh Chauhan Rinu Sharma ranju ralhan Department of Biochemistry All India Institute of Medical SciencesNew Delhi 110029India Department of Biotechnology School of BiotechnologyGuru Gobind Singh Indraprastha UniversityNew Delhi 110075India Department of Otolaryngology-Head and Neck Surgery Joseph and Mildred Sonshine Family Centre for Head and Neck DiseasesMount Sinai HospitalTorontoON M5G 1X5Canada Department of Pathology and Laboratory Medicine Alex Simona Shnaider Laboratory for Molecular OncologyMount Sinai HospitalTorontoON M5G 1X5Canada

AIM： To determine the functional significance of TC21 in esophageal squamous cell carcinoma （ESCC）. METHODS： TC21 siRNA transfection was carried out using Hyperfectamine to knock down TC21, and tran- scripts were analyzed by reverse transcription-poly- merase chain reaction and protein by Western *** demonstrated the effect of TC21 downregulation of cell signaling in esophageal cancer cells by assess- ing the phosphorylation status of its downstream tar- gets, phosphoinositide 3-kinase （PI3K）, phosphatase and tensin homolog （PTEN）, protein kinase B （pAl〈t）, nuclear factor-KB （NF-~B） and cyclinD1 using specific antibodies. Cell survival analysis after cisplatin treat- ment was carried out by cell viability assay and cell cycle analysis using flow cytometry. RESULTS： TC21 knockdown in human ESCC cell line TEl3 cells, showed only a marginal increase （14.2%） in cell death compared with control cells. The expres- sions of the signaling proteins PI3K and pAkt, transcrip- tion factor NF-KB, and cell cycle protein cyclin D1 were markedly decreased in response to TC21 downregula- tion, whereas the level of pPTEN, an antagonist of PI3K, was increased. In addition, we evaluated the potential of TC21 as a putative target for sensitizing ESCC cells to the chemotherapeutic agent cisplatin. Increased cell death （38.4%） was observed in cells treated with cis- platin after TC21 knockdown compared with cells which were treated with cisplatin alone （20% cell death）. CONCLUSION： Results suggest that TC21 mediates its effects via the PI3K-Akt pathway, NF-KB and cyclin D1, and enhances chemoresistance in esophageal cancer cells.

关键词： TC21 Esophageal squamous cell carci-noma siRNA Cisplatin Chemosensitivity

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Mass Spectrometry-Based Proteomics:From Structure and Energetics of Peptide Ions to Prognostic Cancer Biomarkers

Mass Spectrometry-Based Proteomics:From Structure and Energe...

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第五届全国原子光谱及相关技术学术会议

作者： Ajay Matta Leroi V.DeSouza Jason T.K.Hwang ranju ralhan Kenneth P.H.Pritzker K.H.Brian Lam Justin K.-C.Lau Cheuk-Kuen Lai Alan C.Hopkinson K.W.Michael Siu University of Windsor

＜正＞Tandem mass spectrometry（MS/MS）is the enabling technology in mass spectrometry-based *** coupled with a protein database,the MS/MS peak lists can often lead to peptide sequence information and unambiguous identification of the peptides and the proteins from which they *** methodology is effective,mainly due to the redundancy of identification information encoded in the sequence,the generally well-behaving fragmentation chemistry of

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