MiR‐526b targets lncRNA SLC16A1‐AS1 to suppress cell proliferation in triple‐negative breast cancer

Abstract

AbstractThe present study investigated the potential interaction between miR‐526b and lncRNA SLC16A1‐AS1 in triple‐negative breast cancer (TNBC). Expression of miR‐526b and SLC16A1‐AS1 in TNBC tumor tissues and paired nontumor tissues from 60 TNBC patients was detected by real‐time polymerase chain reaction (RT‐qPCR). The interaction between miR‐526b and SLC16A1‐AS1 was evaluated with overexpression experiments, followed by RT‐qPCR. The proliferation and migration of cells were detected with cell counting kit‐8 assay and Transwell assay, respectively. Apoptosis of cells was assessed by cell apoptosis assay. The expression of apoptosis‐related proteins was quantified by Western blot analysis. MiR‐526b was predicted to bind with SLC16A1‐AS1. Overexpression of miR‐526b in TNBC cells decreased the expression levels of SLC16A1‐AS1, while overexpression of SLC16A1‐AS1 did not affect the expression of miR‐526b. In TNBC tissues, miR‐526b was downregulated in TNBC tissues, while SLC16A1‐AS1 was upregulated in TNBC tissues compared to that in nontumor tissues. The expression of SLC16A1‐AS1 and miR‐526b were inversely correlated. In vitro experiments showed that overexpression of SLC16A1‐AS1 promoted cell proliferation and invasion but suppressed cell apoptosis. MiR‐526b played an opposite role and suppressed the function of SLC16A1‐AS1. MiR‐526b is downregulated in TNBC and it targets SLC16A1‐AS1 to regulate proliferation, apoptosis, and invasion of TNBC cells.