BACKGROUND
Autophagy disorders are linked to human cancer, and the details of their mechanisms remain unclear.
OBJECTIVE
To investigate the regulatory role of PRMT5 in autophagy of breast cancer cells.
METHODS
Human breast adenocarcinoma cell lines (MDA-MB-231, MCF7) were cultured. Plasmids of overexpression and down-regulation of PRMT5 were transfected into MDA-MB-231 and MCF7 cells. The MTT assay was used to determine the proliferation of MDA-MB-231 and MCF7 cells. A western blotting assay was used to verify the expression of autophage-associated molecules. Immunofluorescence was applied to observe the expression of GFP-LC3.
RESULTS
The expression of PRMT5 decreased the sensitivity to rapamycin and nutrient deprivation. PRMT5 acts as an oncogene and promotes cell proliferation, influences migration, and stamness. PRMT5 expression elevated the autophagic activity initiated by EBSS and Rapamycin. PRMT5 was necessary and sufficient to enhance stress-induced autophagy. PRMT5 could improve several autophagy-related gene expressions. Atg5 expression could be regulated by activating the PRMT5 and PDCD4 molecule. Regulation of ULK1 expression could be mediated by the PRMT5 molecule.
CONCLUSIONS
PRMT5 influenced multiple stages of autophagy in controlling autophagy and tumorigenesis. Autophagy-related PRMT5 might be a respected target for therapeutic interventions in cancers. This study would provide new ideas for the treatment and selection of breast cancer targets.