CCN1 induces apoptosis in esophageal adenocarcinoma through p53-dependent downregulation of survivin

Tong Dang; Cristina Modak; Xiemei Meng; Jinbao Wu; Reinier Narvaez; Jianyuan Chai

doi:10.1002/jcb.27515

CCN1 induces apoptosis in esophageal adenocarcinoma through p53-dependent downregulation of survivin

J Cell Biochem. 2019 Feb;120(2):2070-2077. doi: 10.1002/jcb.27515. Epub 2018 Sep 11.

Authors

Tong Dang¹, Cristina Modak², Xiemei Meng¹, Jinbao Wu¹, Reinier Narvaez², Jianyuan Chai^{1

2

3}

Affiliations

¹ Inner Mongolia Institute of Digestive Diseases, The Second Affiliated Hospital of Baotou Medical College, Inner Mongolia University of Science and Technology, Baotou, Inner Mongolia, China.
² Laboratory of Gastrointestinal Injury and Cancer, VA Long Beach Healthcare System, Long Beach, California.
³ Department of Medicine, College of Medicine, University of California, Irvine, California.

PMID: 30318638
DOI: 10.1002/jcb.27515

Abstract

Many cancer drugs have been developed to control tumor growth by inducing cancer cell apoptosis. However, several intracellular barriers could fail this attempt. One of these barrier is high expression of survivin. Survivin can interfere caspase activation and thereby abort apoptosis. In this study, we found that CCN1 suppressed the survivin expression in tumor cells of esophageal adenocarcinoma (EAC) and thus allowed apoptosis to finish. Furthermore, we demonstrated that this downregulation was dependent on p53 phosphorylation at Ser20, and CCN1 induced EAC cell apoptosis through the activation of p53.

Keywords: CCN1; apoptosis; esophageal adenocarcinoma (EAC); p53; survivin.

Abstract

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