XEDAR inhibits the proliferation and induces apoptosis of gastric cancer cells by regulating JNK signaling pathway.

Abstract

X-linked ectodermal dysplasia receptor (XEDAR) has been widely studied in epidermal morphogenesis, but few studies have been conducted on tumorigenesis and development, including gastric cancer. In the present research, we aimed to investigate the effect of XEDAR on gastric cancer and further explore the molecular mechanisms involved. The differential expression of XEDAR in 90 tissue specimens (30 gastric cancer tissues, 30 adjacent tissues and 30 normal tissues) was detected by real-time PCR (RT-PCR) and Western blot. Cell proliferation and apoptosis were explored using MTT and Annexin-V/propidium iodide (PI) assays, respectively. The results revealed that the expression of XEDAR was decreased in gastric cancer tissues and in gastric cancer cell lines, and its expression is regulated by p53 in BGC-823 cells. Furthermore, overexpression of XEDAR inhibited cell proliferation and induced apoptosis in BGC-823 cells. XEDAR moreover inhibited proliferation and induced apoptosis in gastric cancer cells by regulating the JNK signaling pathway. Collectively, the results of the present study suggested that XEDAR inhibits cell proliferation and induces apoptosis by participating in p53-mediated signaling pathway and inhibiting the downstream JNK signaling pathway in gastric cancer.

• Authors: Lihong Yang, Xiaojun Huang, Wei Wang, Tao Jiang, Feifei Ding
• Journal: Bioscience reports (Biosci Rep) Vol. 39 Issue 12 (12 20 2019) ISSN: 1573-4935 [Electronic] England
• PMID: 31829409 (Publication Type: Journal Article)
• Copyright: © 2019 The Author(s).

Chemical References

• EDA2R protein, human
• Neoplasm Proteins
• Xedar Receptor
• MAP Kinase Kinase 4

Topics

• Apoptosis
• Cell Line, Tumor
• Cell Proliferation
• Humans
• MAP Kinase Kinase 4 (metabolism)
• MAP Kinase Signaling System
• Neoplasm Proteins (genetics, metabolism)
• Stomach Neoplasms (genetics, metabolism, pathology)
• Xedar Receptor (genetics, metabolism)