DSCAM-AS1 promotes tumor growth of breast cancer by reducing miR-204-5p and upregulatingRRM2

We intended to analyze the effects of DSCAM-AS1, miR-204-5p and RRM2 on breast cancer (BC) cells growth. Microarray analysis and qRT-PCR were employed to determine DSCAM-AS1 and miR-204-5p expression in BC. Luciferase reporter assay and cell transfection assay were applied to examine the target relationship between DSCAM-AS1, miR-204-5p and MMR2. CCK-8 assay, transwell assay and flow cytometry were used to detect cell proliferation, invasion and apoptosis of breast cancer cells. The expression of DSCAM-AS1, miR-204-5p and MMR2 were confirmed by Western Blot. We also conducted In vivo assay to verify the effect of DSCAM-AS1 on tumor formation.DSCAM-AS1 was up-regulated, while miR-204-5p was down-regulated in BC tissues and cells. Meanwhile, DSCAM-AS1 directly targeted miR-204-5p. DSCAM-AS1 promoted the proliferation and invasion of BC cells and restrained cell apoptosis by reducing miR-204-5p and inhibiting miR-204-5p expression. RRM2 was up-regulated in BC cells, and miR-204-5p inhibited RRM2 expression by targeting RRM2 . Overexpression of RRM2 stimulated proliferation and cell invasion and impeded apoptosis of BC cells. In vivo experiments showed that knockdown of DSCAM-AS1 decreased the tumorigenesis of BC cells, increased the expression of miR-204-5p while inhibited RRM2 expression.DSCAM-AS1 promoted proliferation and impaired apoptosis of BC cells by reducing miR-204-5p and enhancing RRM2 expression. DSCAM-AS1/miR-204-5p/ RRM2 may serve as novel therapeutic targets for BC. Summary statement Microarray analysis and qRT-PCR were employed to determine DSCAM-AS1 and miR-204-5p expression in BC. DSCAM-AS1 promoted proliferation and impaired apoptosis of BC cells by reducing miR-204-5p and enhancing RRM2 expression.