MicroRNA-215 acts as a tumor suppressor in breast cancer by targeting AKT serine/threonine kinase 1

Abstract

Abstract. 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.

MicroRNA‑675 inhibits cell proliferation and invasion in melanoma by directly targeting metadherin

“…The identification of the miRNA target genes is important for understanding its roles in carcinogenesis and progression (38). Multiple targets of miR-675 have been identified, including c-Cbl(21), Cbl-b(21) in breast cancer, ZEB1 (34) in pancreatic cancer, GPR55 (33) in non-small cell lung cancer, TGFBI (36) in prostate cancer, CDK6(37) in glioma, p53 (22) in bladder cancer, AKT (32) and Cdc25A (31) in hepatocellular carcinoma.…”

Pax-5 Inhibits Breast Cancer Proliferation Through MiR-215 Up-regulation

“…miR-215; -532; -3619; -489 and -130a) found to influence breast cancer cell processes in the same fashion as does Pax-5. For example, miR-130a, miR-489 and miR-215 have been found to be implicated in cell proliferation and invasion of breast cancer cells (34,35) whereas miR-3619 and miR-532 have been shown to modulate these cancer processes in other types of solid tumors (36)(37)(38)(39). Unfortunately, only miR-215 was validated in our breast cancer cell models conditionally overexpressing Pax-5.…”

Insight into the molecular mechanism of LINC00152/miR‐215/CDK13 axis in hepatocellular carcinoma progression

“…miR‐215 is decreased in various cancers . miR‐215 can repress breast cancer progression by targeting AKT . miR‐215 can inhibit epithelial ovarian cancer progression via regulating NOB1 .…”

“…[28][29][30] miR-215 can repress breast cancer progression by targeting AKT. 31 miR-215 can inhibit epithelial ovarian cancer progression via regulating NOB1. 32 Additionally, UICLM induces colorectal cancer liver metastasis via sponging miR-215 to modulate ZEB2.…”