Eur Rev Med Pharmacol Sci 2019; 23 (7): 2838-2846
DOI: 10.26355/eurrev_201904_17561

LncRNA MAFG-AS1 promotes the aggressiveness of breast carcinoma through regulating miR-339-5p/MMP15

H. Li, G.-Y. Zhang, C.-H. Pan, X.-Y. Zhang, X.-Y. Su

Department of Obstetrics and Gynecology, Shandong Jiyang Public Hospital, Ji’nan, Shandong, China. 1936423807@qq.com


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.

Free PDF Download

To cite this article

H. Li, G.-Y. Zhang, C.-H. Pan, X.-Y. Zhang, X.-Y. Su
LncRNA MAFG-AS1 promotes the aggressiveness of breast carcinoma through regulating miR-339-5p/MMP15

Eur Rev Med Pharmacol Sci
Year: 2019
Vol. 23 - N. 7
Pages: 2838-2846
DOI: 10.26355/eurrev_201904_17561