H Li1, G-Y Zhang, C-H Pan, X-Y Zhang, X-Y Su. 1. Department of Obstetrics and Gynecology, Shandong Jiyang Public Hospital, Ji'nan, Shandong, China. 1936423807@qq.com.
Abstract
OBJECTIVE: The main purposes of this study are to investigate the possible effects of long noncoding RNAs (lncRNAs) MAFG-AS1 on the growth and metastasis of breast carcinoma. PATIENTS AND METHODS: The quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) assay was used to assess the MAFG-AS1 level in breast cancer tissues and cells. The wound healing and transwell invasion analysis were applied to explore the invasion and migration of breast cancer cell in vitro. The expressions of epithelial-mesenchymal transition (EMT) related markers were determined by Western blotting. Xenograft model and lung metastasis model were used to assess the progression of breast carcinoma cell in vivo. RESULTS: The level of lncRNA MAFG-AS1 is higher in breast carcinoma, and the aggressive phenotypes of breast carcinoma cell are enhanced by MAFG-AS1 transfection. Moreover, we identify that MAFG-AS1 overexpression reduces the expression of miR-339-5p and miR-339-5p is the target of MAFG-AS1 in breast carcinoma. In addition, matrix metalloproteinase 15 (MMP15) is the functional regulated gene of miR-339-5p in breast carcinoma. The aggressiveness of breast carcinoma induced by lncRNA MAFG-AS1 is weakened by the miR-339-5p. Finally, we demonstrated that the development of breast carcinoma cell is enhanced by MAFG-AS1 in vivo. CONCLUSIONS: MAFG-AS1 appears to play an oncogene role in breast carcinoma by regulating the miR-339-5p/MMP15.
OBJECTIVE: The main purposes of this study are to investigate the possible effects of long noncoding RNAs (lncRNAs) MAFG-AS1 on the growth and metastasis of breast carcinoma. PATIENTS AND METHODS: The quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) assay was used to assess the MAFG-AS1 level in breast cancer tissues and cells. The wound healing and transwell invasion analysis were applied to explore the invasion and migration of breast cancer cell in vitro. The expressions of epithelial-mesenchymal transition (EMT) related markers were determined by Western blotting. Xenograft model and lung metastasis model were used to assess the progression of breast carcinoma cell in vivo. RESULTS: The level of lncRNA MAFG-AS1 is higher in breast carcinoma, and the aggressive phenotypes of breast carcinoma cell are enhanced by MAFG-AS1 transfection. Moreover, we identify that MAFG-AS1 overexpression reduces the expression of miR-339-5p and miR-339-5p is the target of MAFG-AS1 in breast carcinoma. In addition, matrix metalloproteinase 15 (MMP15) is the functional regulated gene of miR-339-5p in breast carcinoma. The aggressiveness of breast carcinoma induced by lncRNA MAFG-AS1 is weakened by the miR-339-5p. Finally, we demonstrated that the development of breast carcinoma cell is enhanced by MAFG-AS1 in vivo. CONCLUSIONS:MAFG-AS1 appears to play an oncogene role in breast carcinoma by regulating the miR-339-5p/MMP15.