TGF-β induces HLA-G expression through inhibiting miR-152 in gastric cancer cells. Issue 1 (December 2015)

• Record Type: Journal Article
• Authors: Guan, Zhongzheng; Song, Bingtan; Liu, Fengjun; Sun, Dong; Wang, Kexin; Qu, Hui
• Is Part Of: Journal of biomedical science. Volume 22:Issue 1(2015)
• Page Start: 1
• Page End: 7
• Publication Date: 2015-12
• Subjects: Gastric cancer -- miR-152 -- TGF-β -- HLA-G; Medical sciences -- Periodicals; 610.28
• DOI: 10.1186/s12929-015-0177-4
• Languages: English
• ISSNs: 1021-7770

Abstract

Abstract Background Mounting evidences have showed the important role of transforming growth factor-β (TGF-β) in immunological surveillance of tumors. Some studies have also indicated human leukocyte antigen (HLA)-G-associated immune escape involving TGF-β management in gastric cancer (GC). However, the mechanism underlying it is unclear. This study aims to verify the correlations between HLA-G and TGF-β, involving the potential targeting of miR-152 on HLA-G. Results TGF-β and HLA-G levels were analyzed in blood samples from twenty GC patients with ELISA assays, while TGF-β showed directly proportional to HLA-G levels in GC patients, and TGF-β induced HLA-G up-regulation was also confirmed in GC cell lines. Furthermore, miR-152 expression could be inhibited by TGF-β, and the negative post-transcriptionally regulation of miR-152 on HLA-G was also demonstrated through gain- and loss-of-function studies. Besides, miR-152 overexpression repressed HLA-G up-regulation induced by TGF-β. And, miR-152 expression levels showed inversely proportional to both HLA-G and also TGF-β levels in GC patients. Conclusion TGF-β could induce HLA-G expression in GC by inhibiting miR-152, involving its negative regulation on HLA-G. Since TGF-β induced HLA-G up-regulation plays important role in immune escape, a potential application of miR-152 was suggested in GC treatment, or miR-152 might be one potential biomarker for GC.