MicroRNAs (miRNAs or miRs) play crucial roles in human breast cancer. Although miR-1254 has been shown to have oncogenic activity in several cancer types, its biological function in breast cancer and its mechanisms of action remain unclear. In this study, we investigated the role of miR-1254 in human breast cancer and sought to elucidate the relevant underlying mechanisms. We found that miR-1254 expression was markedly increased in breast cancer tissues and cell lines. Additionally, miR-1254 overexpression accelerated breast cancer cell proliferation, cell cycle G1-S phase transition and inhibited apoptosis. Nevertheless, the inhibition of miR-1254 suppressed cell proliferation and induced apoptosis. Further analyses revealed that miR-1254 expression negatively correlated with RASSF9 expression in breast cancer tissues. We verified that RASSF9 was a direct target of miR-1254 using a luciferase reporter assay. The overexpression of miR-1254 reduced the RASSF9 mRNA and protein levels, and the suppression of miR-1254 promoted RASSF9 expression. Notably, the knockdown or overexpression of RASSF9 corroborated the biological effects observed upon miR-1254 overexpression or inhibition. Taken together, these results demonstrate that miR-1254 accelerates breast cancer cell growth by activating the AKT signaling pathway and suppresses apoptosis by inhibiting p53 expression through the targeting of RASSF9. The data indicate that miR-1254 plays a crucial role in human breast cancer, and may represent a novel therapeutic target for this malignancy.

The Ras-association domain family (RASSF) proteins have been involved in many important biological processes. RASSF7 is recently reported to be up-regulated in several types of cancer. However, the function of RASSF7 remain unknown in human cancers. To explore the role of RASSF7 in hepatocellular carcinoma (HCC) cells proliferation and molecular mechanism. RASSF7 expression was examined using public database TCGA, qRT-PCR and Western blot. The correlation between RASSF7 and clinicopathological features was measured. Overexpression and silencing of RASSF7 were performed to measure the impact on HCC cell proliferation, cell cycle and apoptosis. Futhermore, the molecular mechanism of MEK1/2-ERK1/2 signaling pathway regulation by RASSF7 was explored. RASSF7 was significantly up-regulated in HCC tissues and cell lines, and correlated with AFP, poor tumor histology and T stage. Overexpression of RASSF7 promoted HCC cell proliferation, drived G1-S phase cell cycle transition and inhibited apoptosis. Knockdown of RASSF7 suppressed cell growth, induced G1-S phase cell cycle arrest and cell apoptosis. Furthermore, our findings also demonstrated that RASSF7 promoted HCC cell proliferation through activating MEK1/2-ERK1/2 signaling pathway. Taken together, this study provides a novel evidence for clinical significance of RASSF7 as a potential biomarker, and demonstrates that RASSF7- MEK1/2-ERK1/2 signaling pathway might be a novel pathway involved in HCC progression.