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Micro RNA ‐645 promotes metastasis of osteosarcoma via targeting tumor suppressor NM 23 nucleoside diphosphate kinase 2
Author(s) -
Jiao GuangJun,
Zhang ShiJun,
Li Yi,
Wu WenLiang,
Liu HaiChun
Publication year - 2018
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/1440-1681.13006
Subject(s) - osteosarcoma , cancer research , gene knockdown , metastasis , microrna , gene silencing , nucleoside diphosphate kinase , medicine , chemistry , kinase , pathology , cell culture , biology , cancer , gene , biochemistry , genetics
Summary Osteosarcoma is the most common non‐hematological primary bony malignancy in children and young adults with tumor metastasis being a common event at diagnosis. Understanding the pathogenesis of metastatic osteosarcoma may help identify potential therapeutic targets. In this study, we found that the level of microRNA‐645 (miR‐645) in osteosarcoma tumor tissues was significantly increased compared with their paired non‐tumorous tissues, and was associated with histologic grade, TNM staging, lymph metastasis and distant metastasis. Knockdown of miR‐645 caused a remarkable inhibition of migration of osteosarcoma U2 OS cells. Furthermore, miR‐645 inhibited NME 2 (nucleoside diphosphate kinase 2) expression through directly binding to its 3′ untranslated region. In human osteosarcoma tissues, we also found that NME 2 was significantly decreased in tumor tissues, and its level was negatively correlated with miR‐645. In addition, silencing NME 2 attenuated the decreased cell migration by knockdown of miR‐645, suggesting that it was involved in the miR‐645 induced cell migration of osteosarcoma cells. Taken together, we found that miR‐645 was up‐regulated in osteosarcoma tissues and could promote osteosarcoma cell migration through directly inhibiting the tumor suppressor NME 2. Our data provide novel insight into the role of miR‐645 in osteosarcoma and indicate that miR‐645 might be a potential therapeutic target of osteosarcoma.