摘要
Studies have proved that microRNA-101 （miR-101） functions as a tumor suppressor and is associated with growth and apoptosis of various human cancers. However, the role of miR-101 in os- teosarcoma and the possible mechanism by which miR-101 affects the tumor growth and apoptusis have not been fully elucidated. In this study, we found that the expression ofmiR-101 was down-regulated in osteosarcoma tissues and Saos-2 cell line as compared with that in adjacent non-neoplastic bone tissues and the osteoblastic cell line. To better characterize the role of miR-101 in osteosarcoma, we used a gain-of-function analysis by transfecting human osteosarcoma cell line Saos-2 with chemically synthe- sized miR-101 mimics. The results showed that overexpression of miR-101 inhibited the proliferation and promoted the apoptosis of Saos-2 cells. Meanwhile, bioinformatic analysis demonstrated that mTOR gene was a direct target of miR- 101. Overexpression of miR- 101 significantly decreased the ex- pression of roTOR at both mRNA and protein levels in Saos-2 cells, consequently inhibiting Saos-2 cells proliferation and promoting ceils apoptosis in an mTOR-dependent manner. Taken together, these data suggest that miR-101 may act as a tumor suppressor, which is commonly downregulated in both osteosarcoma tissues and cells, roTOR plays an important role in mediating miR-101 dependent bio- logical functions in osteosarcoma. Reintroduction of miR-101 may be a novel therapeutic strategy bydown-regulating mTOR expression.
Studies have proved that microRNA-101 （miR-101） functions as a tumor suppressor and is associated with growth and apoptosis of various human cancers. However, the role of miR-101 in os- teosarcoma and the possible mechanism by which miR-101 affects the tumor growth and apoptusis have not been fully elucidated. In this study, we found that the expression ofmiR-101 was down-regulated in osteosarcoma tissues and Saos-2 cell line as compared with that in adjacent non-neoplastic bone tissues and the osteoblastic cell line. To better characterize the role of miR-101 in osteosarcoma, we used a gain-of-function analysis by transfecting human osteosarcoma cell line Saos-2 with chemically synthe- sized miR-101 mimics. The results showed that overexpression of miR-101 inhibited the proliferation and promoted the apoptosis of Saos-2 cells. Meanwhile, bioinformatic analysis demonstrated that mTOR gene was a direct target of miR- 101. Overexpression of miR- 101 significantly decreased the ex- pression of roTOR at both mRNA and protein levels in Saos-2 cells, consequently inhibiting Saos-2 cells proliferation and promoting ceils apoptosis in an mTOR-dependent manner. Taken together, these data suggest that miR-101 may act as a tumor suppressor, which is commonly downregulated in both osteosarcoma tissues and cells, roTOR plays an important role in mediating miR-101 dependent bio- logical functions in osteosarcoma. Reintroduction of miR-101 may be a novel therapeutic strategy bydown-regulating mTOR expression.
