There are accumulating reports that
microRNAs are dysregulated in a number of human
cancer types, and that they may function as
tumor suppressors or oncogenes in
tumorigenesis and
tumor development. microRNA-215 (miR-215) has been identified as a
tumor suppressor in epithelial ovarian, pancreatic, non-small cell lung and
colon cancer, whereas it may act as an oncogene in gastric and
cervical cancer. The role of miR-215 in
breast cancer carcinogenesis and progression has yet to be elucidated. In the present study, the expression level of miR-215 was determined in
breast cancer tissues and cell lines using the reverse transcription-quantitative polymerase chain reaction. The effects of miR-215 overexpression on proliferation and the invasive capacity of
breast cancer cells were assessed using MTT and cell invasion assays. The results revealed that miR-215 was significantly downregulated in
breast cancer tissues and cell lines. Restoration of miR-215 expression inhibited the proliferation and invasion of
breast cancer cells. The underlying molecular mechanism for the suppression of proliferation and invasion by miR-215 was investigated. AKT
serine/threonine kinase 1 (AKT1) was validated as a novel direct target of miR-215, and the effect of AKT1
small interfering RNA mimicked the effect of miR-215 overexpression in
breast cancer cells. These results indicated that miR-215 acted as a
tumor suppressor, and that its downregulation in
tumor tissues may contribute to the
carcinogenesis and progression of
breast cancer, indicating that miR-215 may be a novel therapeutic target for the treatment of
breast cancer.