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Although SLC16A1-AS1 is involved in lung cancer, its function in breast cancer is still elusive. We observed downregulation of SLC16A1-AS1 expression in triple-negative breast cancer (TNBC) by analyzing TCGA dataset. Therefore, we analyzed the function of SLC16A1-AS1 in TNBC. We observed downregulation of SLC16A1-AS1 expression in TNBC by analyzing TCGA dataset. Therefore, we analyzed the function of SLC16A1-AS1 in TNBC. SLC16A1-AS1 expression was downregulated in TNBC tissues. SLC16A1-AS1 interacted with miR-182, whereas SLC16A1-AS1 and miR-182 overexpression failed to affect their expression. SLC16A1-AS1 overexpression upregulated the expression of PDCD4, a downstream target of miR-182. SLC16A1-AS1 and PDCD4 overexpression suppressed cell cycle progression from the G1 phase to the G2 phase. MiR-182 and silencing of PDCD4 played the opposite role. Additionally, miR-182 overexpression inhibited the role of SLC16A1-AS1 overexpression on cell cycle progression in both BT-549 and BT20 cells. The cell proliferation assay showed that SLC16A1-AS1 and PDCD4 overexpression decreased the cell proliferation rate. SLC16A1-AS1 may inhibit cell cycle progression and restrain TNBC cell proliferation by regulating the miR-182/PDCD4 axis.

LncRNA SLC16A1-AS1 regulates the miR-182/PDCD4 axis and inhibits the triple-negative breast cancer cell cycle