Stromal interaction molecule 1 promotes tumor growth in Esophageal squamous cell carcinoma
Esophageal squamous cell carcinoma (ESCC) is a disease with poor prognosis which urgently is in need of effective prognostic marker. To discover novel prognostic protein marker for ESCC, we applied a high-throughput monoclonal antibody microarray to compare tumor and adjacent non-tumor tissues from...
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Published in | Genomics (San Diego, Calif.) Vol. 112; no. 3; pp. 2146 - 2153 |
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Main Authors | , , , , , |
Format | Journal Article |
Language | English |
Published |
United States
Elsevier Inc
01.05.2020
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Subjects | |
Online Access | Get full text |
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Summary: | Esophageal squamous cell carcinoma (ESCC) is a disease with poor prognosis which urgently is in need of effective prognostic marker. To discover novel prognostic protein marker for ESCC, we applied a high-throughput monoclonal antibody microarray to compare tumor and adjacent non-tumor tissues from ESCC patients. Antibody #ESmAb270 was consistent higher expressed in tumors and it was identified via mass spectrometry to be stromal interaction molecule 1 (STIM1). STIM1 H scores in tumor tissues were significantly up-regulated in esophageal tumor tissues compared to non-tumor tissues in 105 ESCC patients. We also observed that high STIM1 expression was correlated with advanced tumor grade and poor prognosis of ESCC. In addition, attenuation of STIM1 by siRNA or chemical inhibitors significantly inhibited cell viability and migration of ESCC cells. Evidence from high-throughput monoclonal antibody microarray, IHC microarray with associated survival data and functional analysis show that STIM1 is an unfavorable prognostic biomarker in ESCC.
•Antibody microarray is a unique approach to identify differentially expressed proteins.•STIM1 was found to be up-regulated in esophageal squamous cell carcinoma.•STMI1 expression is associated with poor survival in esophageal squamous cell carcinoma.•Attenuation of STIM1 by siRNA inhibited cell viability and migration of esophageal squamous cell carcinoma cells. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0888-7543 1089-8646 |
DOI: | 10.1016/j.ygeno.2019.12.008 |