Research Papers:
Correlation of clinical features and genetic profiles of stromal interaction molecule 1 (STIM1) in colorectal cancers
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Abstract
Henry Sung-Ching Wong1,2, Wei-Chiao Chang1,2,3,4,5
1Master Program for Clinical Pharmacogenomics and Pharmacoproteomics, School of Pharmacy, Taipei Medical University, Taipei, Taiwan
2Department of Clinical Pharmacy, School of Pharmacy, Taipei Medical University, Taipei, Taiwan
3Department of Pharmacy, Taipei Medical University Wan Fang Hospital, Taipei, Taiwan
4Center for Biomarkers and Biotech Drugs, Kaohsiung Medical University, Kaohsiung, Taiwan
5Department of Pharmacy, Taipei Medical University Wan Fang Hospital, Taipei, Taiwan
Correspondence to:
Wei-Chiao Chang, e-mail: [email protected]
Keywords: colorectal cancer, stored-operated calcium entry pathway, stromal interaction molecule 1, bioinformatics, data mining
Received: July 21, 2015 Accepted: October 22, 2015 Published: November 03, 2015
ABSTRACT
STIM1 overexpression has been observed in a portion of colorectal cancer (CRC) patients and associated with cancer cell invasion and migration. To characterize the distinctive expression profiles associated with stromal interaction molecule 1 (STIM1) overexpression/low-expression between CRC subtypes, and further assess the divergence transcription regulation impact of STIM1 between colon (COADs) and rectum (READs) adenocarcinomas in order to depict the role of SOCE pathway in CRCs, we have conducted a comprehensive phenome-transcriptome-interactome analysis to clarify underlying molecular differences of COADs/READs contributed by STIM1. Results demonstrated that a number of novel STIM1-associated signatures have been identified in COADs but not READs. Specifically, the presence of STIM1 overexpression in COADs, which represented a disturbance of the SOCE pathway, was associated with cell migration and cell motility properties. We identified 11 prognostic mRNA/miRNA predictors associated with the overall survival of COAD patients, suggesting the correlation of STIM1-associated features to clinicopathological outcomes. These findings enhance our understanding on differences between CRC subtypes in panoramic view, and suggested STIM1 as a promising therapeutic biomarker in COADs.
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