LncRNA MAFG-AS1 deregulated in breast cancer affects autophagy and progression of breast cancer by interacting with miR-3612 and FKBP4 invitro

• Published in: Biochemical and biophysical research communications Vol. 616; pp. 95 - 103
• Main Authors: Gao, Zhaoxia, Zheng, Gang, Gong, Xiaojun, Hu, Han, Shao, Liwei, Pang, Yan, Wang, Yirui, Qi, Aihong
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 06-08-2022
• Subjects: Breast cancer; FKBP4; MAFG-AS1; miR-3612; Breast cancer; FKBP4; miR-3612; MAFG-AS1
• ISSN: 0006-291X; 1090-2104
• DOI: 10.1016/j.bbrc.2022.05.020

We aimed to explore the function and competing endogenous RNA (ceRNA) pathway of MAFG-AS1 in breast cancer.
qRT-PCR assay identified the expression of MAFG-AS1, miR-3612 and FKBP4. We used Western blot analysis to test the autophagy related protein levels in breast cancer cells. Functional assays such as Cell Counting Kit-8 (CCK8) assay, BrdU proliferation assay, Caspase-3 activity detection were used to identify the function of MAFG-AS1, miR-3612 and FKBP4 in breast cancer cells. Mechanism assays were used to verify the interacting relationship among MAFG-AS1, miR-3612 and FKBP4, including RNA pull down assay, RNA immunoprecipitation (RIP) assay and luciferase reporter assay.
MAFG-AS1 and FKBP4 were both up-regulated in breast cancer tissues. MAFG-AS1 could function as an oncogene in breast cancer to activate cell proliferation, and inhibit cell apoptosis and autophagy. Meanwhile, MAFG-AS1 could sponge miR-3612 to elevate the expression of FKBP4. Besides, FKBP4 could activate the cell proliferation and inhibit cell apoptosis and autophagy, which could relieve the inhibitory effect of miR-3612 on breast cancer cells.
MAFG-AS1 could activate breast cancer progression via modulating miR-3612/FKBP4 axis in vitro.
•Bioinformatics analysis was done to select the study objects.•The binding between MAFG-AS1 and miR-3612 was proved in BRCA cells.•MAFG-AS1/miR-3612 axis could modulate the progression of BRCA in vitro.•MiR-3612 could target FKBP4 in BRCA cells.