Abstract. ) is expressed at lower levels in prostate cancer cells compared with normal prostate cells. However, the regulatory mechanism of miR-26a in tumorigenesis and metastasis is not clear. In the present study, the expression profile of cellular miR-26a was analyzed by reverse transcription-quantitative polymerase chain reaction. The potential target of miR-26a was identified by luciferase assay and western blotting. Examination of miR-26a function was performed by transfection with miR-26a mimics and inhibitor. It was found that miR-26a expression was decreased in prostate cancer tissues and cell lines, with androgen-independent prostate cancer (AIPC) showing lower miR-26a expression compared with androgen-dependent prostate cancer (ADPC). Overexpression of miR-26a by transfecting miR-26a mimics could significantly enhance apoptosis, and this upregulation of apoptosis was triggered by cytochrome c oxidase subunit II inhibition. Furthermore, it was found that lower miR-26a density resulted in an evidently poor prognosis. Understanding the important roles of miR-26a in regulating cell apoptosis in human prostate cancer cells may aid the exploration of AIPC transformation mechanisms and contribute to the development of miRNA-based therapy in the future.

ABSTRACT. Osteosarcoma (OS) causes millions of death worldwide and, since there is no effective therapy, it is necessary to identify the molecular mechanism of OS, which can direct the development of new therapies. This study investigated the role of bone morphogenetic protein 9 (BMP9), a member of the transforming growth factor (TGF)-β family, in OS development. This study first examined BMP9 expression in tissue from OS patients and normal subjects. The OS cell line (MG63) and tumor cells from OS patients were then transfected with BMP9 and cell proliferation and apoptosis were assessed. Western blot and reverse transcription-polymerase chain reaction were used to study the expression of cancer-related genes [B cell lymphoma (Bcl)-2, cleaved Caspase-3, Caspase-9, and poly ADP-ribose polymerase]. To confirm the in vivo impact of BMP9, mice were transplanted with OS tumor cells and then treated with BMP9 carried in attenuated Salmonella enterica serovar Typhimurium. Our study found that the OS tumor tissue had a lower expression of BMP9 compared to normal tissue. Transfection of BMP9 in OS and MG63 cells inhibited cell growth and promoted apoptosis. In vitro studies showed a decrease in Bcl-2 gene expression and an increase in Cyto-c, Caspase-3, and Caspase-9 expression. In vivo studies indicated that consistent treatment with BMP9 in OS mice results in inhibition of tumor growth. This study shows that BMP9 inhibition is associated with OS development and that enhanced expression of BMP9 may be a potential treatment method for OS.