LINC02381 aggravates breast cancer through the miR-1271-5p/FN1 axis to activate PI3K/AKT pathway

Emerging investigations have demonstrated that lncRNAs are key crucial modulators in cancer. In this study, we investigated the role of LINC02381 in breast cancer (BC). Reverse transcriptase quantitative polymerase chain reaction measured the LINC02381 level in BC tissues and cells. Colony formation, EdU staining, wound healing and Transwell experiments examined the impact of LINC02381 depletion on BC cell phenotypes. Relationship among miR-1271-5p, LINC02381, and FN1 was tested through applying RIP, luciferase reporter, and RNA pull-down assays. We found that LINC02381 expression was elevated in BC. Functionally, LINC02381 knockdown hampered BC cell proliferation, migration, and invasion. LINC02381 overexpression accelerated tumor formation in vivo. Mechanistically, LINC02381 acted as a ceRNA to increase FN1 via decoying miR-1271-5p. Additionally, LINC02381 activated PI3K/AKT pathway by upregulating FN1. Rescue assays indicated that FN1 upregulation or PI3K/AKT activation rescued the LINC02381 knockdown-mediated inhibition on malignant phenotypes of BC cells. Overall, LINC02381 exerts carcinogenic effects in BC by the miR-1271-5p/FN1 axis to activate PI3K/AKT pathway.