MicroRNA-214 regulates osteosarcoma survival and growth by directly targeting phosphatase and tensin homolog.
نویسندگان
چکیده
An increasing number of microRNAs (miRNAs) have been identified as diagnostic and prognostic biomarkers, as well as additional therapeutic tools, in skeletal diseases. Recent studies have established the pathophysiological role of miR‑214, using human osteoporotic bone specimens. However, miR‑214 expression levels and the underlying regulatory mechanism in human osteosarcoma remain unclear. Quantitative polymerase chain reaction (qPCR) was used to examine the expression of miR‑214 in human osteosarcoma tissues and cells. Transfection of the cells with either a miR‑214 expressing‑plasmid, mimic or inhibitor was performed, in order to investigate the role of miR‑214 in osteosarcoma. In this study, miR‑214 was shown to be significantly increased in the majority of 15 examined osteosarcoma tissues and in the Saos‑2 human osteosarcoma cell line. Overexpression of miR‑214 in Saos‑2 cells induced cell proliferation, while inhibition of miR‑214 promoted Saos‑2 cell apoptosis in vitro. Furthermore, ectopic expression of miR‑214 markedly promoted osteosarcoma development in a subcutaneous xenotransplantation model in BALB/c athymic nude mice. The role of miR‑214 in osteocarcinogenesis was further investigated and phosphatase and tensin homolog (PTEN) was determined to be a direct target of miR‑214 in Saos‑2 cells. The proliferation‑promoting effect of PTEN knockdown was similar to that of miR‑214 overexpression. This study revealed that miR‑214 exerted a crucial role in promoting osteosarcoma progression and this suggests that modulation of miR‑214 levels may provide a novel therapeutic approach in cancer treatment.
منابع مشابه
Inhibition of miR-214 in OS cell lines markedly suppressed cell proliferation, migration and invasion. Phosphatase and tensin homolog (PTEN) was identified as a direct target of miR-214, and ectopic expression of miR-214 inhibited PTEN
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ورودعنوان ژورنال:
- Molecular medicine reports
دوره 10 6 شماره
صفحات -
تاریخ انتشار 2014