| Literature DB >> 28736328 |
Hainan Zhao1, Ying Cheng1, Suhe Dong1, Jicong Du1, Fu Gao1, Ding Sun1, Jianguo Cui1, Jin Ni2, Jianming Cai3.
Abstract
MicroRNA-143 has been implicated in tumor metastasis by directly targeting Bcl-2, and microRNA-143 expression is decreased in several human tumors. However, the expression and targets of miR-143 in radiation carcinogenesis remain unclear. We found that the expression of miR-143 is down-regulated and the expression of B7H1 (Pdcd1) is up-regulated in radiation-induced thymic lymphoma model in BALB/c mice. Additionally, overexpression of miR-143 strongly inhibited cell proliferation and increased cell apoptosis and its down-regulation promoted cell proliferation and reduced cell apoptosis. We also determined that there is an inverse correlation between miR-143 expression and B7H1 protein expression in radiation-induced thymic lymphoma samples, and miR-143 targets B7H1 in a 3'UTR-dependent manner. In addition, we found that adenovirus over-expression of pre-miR-143 reduced tumorigenesis in vivo. Finally, we conclude that down-regulated expression of miR-143 and up-regulation of its direct target B7H1 may indicate a novel therapeutic method for radiation-induced thymic lymphoma by increased expression of miR-143 or inhibition of B7H1.Entities:
Keywords: B7H1; Radiation carcinogenesis; Radiation induced thymic lymphoma (RITL); Tumor therapy; miR-143
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Year: 2017 PMID: 28736328 DOI: 10.1016/j.toxlet.2017.07.891
Source DB: PubMed Journal: Toxicol Lett ISSN: 0378-4274 Impact factor: 4.372