Abstract

Nuclear receptor coactivator 1 (NCOA1) plays crucial roles in the regulation of gene expression mediated by a wide spectrum of steroid receptors such as androgen receptor (AR), estrogen receptor α (ER α), and estrogen receptor β (ER β). Therefore, dysregulations of NCOA1 have been found in a variety of cancer types. However, the clinical relevance and the functional roles of NCOA1 in human esophageal squamous cell carcinoma (ESCC) are less known. We found in this study that elevated levels of NCOA1 protein and/or mRNA as well as amplification of the NCOA1 gene occur in human ESCC. Elevated levels of NCOA1 due to these dysregulations were not only associated with more aggressive clinic‐pathologic parameters but also poorer survival. Results from multiple cohorts of ESCC patients strongly suggest that the levels of NCOA1 could serve as an independent predictor of overall survival. In addition, silencing NCOA1 in ESCC cells remarkably decreased proliferation, migration, and invasion. These findings not only indicate that NCOA1 plays important roles in human ESCC but the levels of NCOA1 also could serve as a potential prognostic biomarker of ESCC and targeting NCOA1 could be an efficacious strategy in ESCC treatment.

Highlights

  • We found that Nuclear receptor coactivator 1 (NCOA1) is highly enriched in human esophageal squamous cell carcinoma (ESCC), and the levels of NCOA1 are clinically important in ESCC progression and patient prognosis

  • Given the fact that dysregulation of NCOA1 was found in multiple types of cancers, we were interested in knowing if this coactivator plays any role in ESCC

  • We conducted a tissue microarray (TMA) to compare the NCOA1 protein levels in ESCC specimens with their adjacent non‐tumor tissues (ANT) from 80 ESCC patients

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Summary

Funding information

The Department of Education, Guangdong Government under the Top‐tier University Development Scheme for Research and Control of Infectious Diseases; Li Ka Shing Foundation Grant for Joint Research Program between Shantou University and Technion‐Israel Institute of Technology, Shantou University, Guangdong Province; The funding for Collaborative and Creative Center, Molecular Diagnosis and Personalized Medicine; National Natural Science Foundation of China, Grant/ Award Number: 30973508; Li Ka Shing

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