Objective To investigate the role and potential mechanism of long non-coding RNA sequence similarity family 83 member A-antisense ribonucleic acid 1 ( lncRNA FAM83A-AS1) in breast cancer (BC). Methods The expression of FAM83A in BC tissue was detected by immunohistochemistry, and lncRNA FAM83A-AS1 and FAM83A mRNA in BC tissues/ cells was detected by real-time fluorescent quantitative PCR (qRT-PCR). Pearson method was employed to test the correlation between lncRNA FAM83A-AS1 and FAM83A mRNA expression levels in BC tissues. Cell transfection silencing of MDA-MB-231 was used to study gene overexpression. The expression levels of lncRNA FAM83AAS1 and FAM83A mRNA in MDA-MB-231 cells were detected by qRT-PCR. MDA-MB-231 cell proliferation activity was detected via the CCK-8 method. MDA-MB-231 cell migration and invasion abilities were detected by Transwell experiment. The protein expression of FAM83A, ERK1 / 2 and its phosphorylated protein Ki-67, E-cadherin and matrix metalloproteinase 9 in MDA-MB-231 cells was detected by Western blot. The subcellular distribution of lncRNA FAM83AAS1 was detected by nucleocytoplasmic separation experiments, and the interaction between lncRNA FAM83A-AS1 and FAM83A was verified by RNA pull-down, RNA immunoprecipitation (RIP) and qRT-PCR assays. Nude mice were used in a tumorigenesis experiment to detect the effect of lncRNA FAM83A-AS1 silencing on the growth of MDA-MB-231 cells in vivo. We employed immunohistochemistry staining to detect the expression of Ki-67 and FAM83A in tumors. Results The expression of lncRNA FAM83A-AS1 and FAM83A mRNA in BC tissues and cells was significantly up-regulated ( P<0. 05). Pearson analysis showed that the expression levels of lncRNA FAM83A-AS1 and FAM83A mRNA in BC tissues were positively correlated (r= 0. 885, P<0. 05). LncRNA FAM83A-AS1 silencing reduced the proliferation of MDA-MB-231 cells; inhibited the migration and invasion of MDA-MB-231 cells; promoted E-cadherin expression; inhibited FAM38A, Ki-67 and matrix metalloproteinase 9 expression and ERK1 / 2 activation; and inhibited the growth of transplanted tumors in nude mice (P<0. 05). Up-regulating the expression of FAM83A significantly reduced the inhibitory effects of lncRNA FAM83A-AS1-silencing on proliferation, migration, and invasion by MDA-MB-231 cells (P< 0. 05). LncRNA FAM83A-AS1 is present in both the nucleus and cytoplasm and can bind to FAM83A through the RNA-binding protein FBL to increase the expression of FAM83A. Conclusions LncRNA FAM83A-AS1 can promote proliferation,migration, and invasion by MDA-MB-231 cells by up-regulating FAM83A expression.