长链非编码 RNA SLC16A1-AS1 通过调控 miR-182/PDCD4 轴抑制三阴性乳腺癌细胞周期。
LncRNA SLC16A1-AS1 regulates the miR-182/PDCD4 axis and inhibits the triple-negative breast cancer cell cycle.
机构信息
Department of Pathology, Liaoning Cancer Hospital and Institute, Cancer Hospital of China Medical University, Shenyang, PR China.
Department of Pathology, College of Basic Medical Sciences, China Medical University, Shenyang, PR China.
出版信息
Immunopharmacol Immunotoxicol. 2022 Aug;44(4):534-540. doi: 10.1080/08923973.2022.2056482. Epub 2022 May 2.
PURPOSE
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.
METHODS
We observed downregulation of SLC16A1-AS1 expression in TNBC by analyzing TCGA dataset. Therefore, we analyzed the function of SLC16A1-AS1 in TNBC.
RESULTS
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.
CONCLUSION
SLC16A1-AS1 may inhibit cell cycle progression and restrain TNBC cell proliferation by regulating the miR-182/PDCD4 axis.
目的
虽然 SLC16A1-AS1 参与了肺癌的发生，但它在乳腺癌中的作用仍不清楚。通过分析 TCGA 数据集，我们观察到三阴性乳腺癌（TNBC）中 SLC16A1-AS1 的表达下调。因此，我们分析了 SLC16A1-AS1 在 TNBC 中的功能。
方法
通过分析 TCGA 数据集，我们观察到 TNBC 中 SLC16A1-AS1 的表达下调。因此，我们分析了 SLC16A1-AS1 在 TNBC 中的功能。
结果
SLC16A1-AS1 在 TNBC 组织中表达下调。SLC16A1-AS1 与 miR-182 相互作用，而 SLC16A1-AS1 和 miR-182 的过表达未能影响其表达。SLC16A1-AS1 的过表达上调了 miR-182 的下游靶基因 PDCD4 的表达。SLC16A1-AS1 和 PDCD4 的过表达抑制了细胞从 G1 期到 G2 期的周期进程。miR-182 和 PDCD4 的沉默则起到了相反的作用。此外，miR-182 的过表达抑制了 SLC16A1-AS1 过表达对 BT-549 和 BT20 细胞周期进程的作用。细胞增殖实验表明，SLC16A1-AS1 和 PDCD4 的过表达降低了细胞的增殖速率。
结论
SLC16A1-AS1 可能通过调节 miR-182/PDCD4 轴抑制细胞周期进程并抑制 TNBC 细胞增殖。
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