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CCN1 sensitizes esophageal cancer cells to TRAIL-mediated apoptosis.

Authors
  • Dang, Tong1
  • Modak, Cristina2
  • Meng, Xiemei1
  • Wu, Jinbao1
  • Narvaez, Reinier2
  • Chai, Jianyuan3
  • 1 The Second Affiliated Hospital of Baotou Medical College, Inner Mongolia University of Science and Technology, 30 Hudemulin Rd, Baotou 014030, China. , (China)
  • 2 Laboratory of Gastrointestinal Injury and Cancer, VA Long Beach Healthcare System, Long Beach, CA 90822, USA.
  • 3 The Second Affiliated Hospital of Baotou Medical College, Inner Mongolia University of Science and Technology, 30 Hudemulin Rd, Baotou 014030, China; Laboratory of Gastrointestinal Injury and Cancer, VA Long Beach Healthcare System, Long Beach, CA 90822, USA; College of Medicine, University of California Irvine, CA 92697, USA. Electronic address: [email protected] , (China)
Type
Published Article
Journal
Experimental Cell Research
Publisher
Elsevier
Publication Date
Dec 01, 2017
Volume
361
Issue
1
Pages
163–169
Identifiers
DOI: 10.1016/j.yexcr.2017.10.015
PMID: 29055676
Source
Medline
Keywords
License
Unknown

Abstract

TRAIL is one of the best anti-cancer molecules in our body. It kills a variety of cancer cells that are resistant to conventional chemotherapy, without causing much negative impact on normal cells, because its death receptors are almost exclusively found on cancer cells. However, some cancer cells are not sensitive to TRAIL treatment, even though they express its death receptors. A second molecule is needed to help TRAIL to complete its mission. Finding such molecules now becomes a top priority in cancer research. Our study shows that CCN1 is such a molecule. CCN1 was highly expressed in the esophageal epithelium of the patients suffering from gastroesophageal reflux disease, but faded away as the situation worsened towards adenocarcinoma. Treating the tumor cells with CCN1 resulted in apoptosis, while the same treatment to the normal cells only nourished cell growth. It was TRAIL that mediated this process. Apparently, CCN1 altered the expression profile of TRAIL and its receptors in tumor cells, namely, activating TRAIL and its death receptors and shutting down its decoy receptors. CCN1 and TRAIL worked as a team to put the cancer cells to death, as elimination of either one failed apoptosis.

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