The 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.

中文翻译：

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MiR-526b 靶向 lncRNA SLC16A1-AS1 抑制三阴性乳腺癌细胞增殖

本研究调查了 miR-526b 和 lncRNA SLC16A1-AS1 在三阴性乳腺癌 (TNBC) 中的潜在相互作用。通过实时聚合酶链反应 (RT-qPCR) 检测 miR-526b 和 SLC16A1-AS1 在来自 60 名 TNBC 患者的 TNBC 肿瘤组织和配对的非肿瘤组织中的表达。通过过表达实验评估 miR-526b 和 SLC16A1-AS1 之间的相互作用，然后进行 RT-qPCR。分别用cell counting kit-8 assay和Transwell assay检测细胞增殖和迁移情况。通过细胞凋亡测定评估细胞的凋亡。通过蛋白质印迹分析定量细胞凋亡相关蛋白的表达。预计 MiR-526b 会与 SLC16A1-AS1 结合。TNBC 细胞中 miR-526b 的过表达降低了 SLC16A1-AS1 的表达水平，而SLC16A1-AS1过表达不影响miR-526b的表达。在 TNBC 组织中，与非肿瘤组织相比，miR-526b 在 TNBC 组织中下调，而 SLC16A1-AS1 在 TNBC 组织中上调。SLC16A1-AS1 和 miR-526b 的表达呈负相关。体外实验表明，SLC16A1-AS1的过表达促进细胞增殖和侵袭，但抑制细胞凋亡。MiR-526b起到了相反的作用，抑制了SLC16A1-AS1的功能。MiR-526b 在 TNBC 中下调，它靶向 SLC16A1-AS1 以调节 TNBC 细胞的增殖、凋亡和侵袭。SLC16A1-AS1 和 miR-526b 的表达呈负相关。体外实验表明，SLC16A1-AS1的过表达促进细胞增殖和侵袭，但抑制细胞凋亡。MiR-526b起到了相反的作用，抑制了SLC16A1-AS1的功能。MiR-526b 在 TNBC 中下调，它靶向 SLC16A1-AS1 以调节 TNBC 细胞的增殖、凋亡和侵袭。SLC16A1-AS1 和 miR-526b 的表达呈负相关。体外实验表明，SLC16A1-AS1的过表达促进细胞增殖和侵袭，但抑制细胞凋亡。MiR-526b起到了相反的作用，抑制了SLC16A1-AS1的功能。MiR-526b 在 TNBC 中下调，它靶向 SLC16A1-AS1 以调节 TNBC 细胞的增殖、凋亡和侵袭。