Department of Preventive Health, The Fourth Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150001, P.R. China.
Department of Thoracic Surgery, First Hospital of Qiqihar City, Qiqihar, Heilongjiang 161000, P.R. China.
Mol Med Rep. 2020 Mar;21(3):1509-1516. doi: 10.3892/mmr.2020.10944. Epub 2020 Jan 16.
Cancer cells use aerobic glycolysis to sustain their proliferation. Long non‑coding RNA brain cytoplasmic RNA 1 (BCYRN1) has been reported to act as an oncogene in non‑small‑cell lung cancer (NSCLC). The present study investigated the role of BCYRN1 in NSCLC glycolysis. BCYRN1 expression was detected in NSCLC cells and tissues using reverse transcription‑quantitative PCR. The effect of BCYRN1 on aerobic glycolysis was examined by measuring NSCLC cell glucose catabolism and lactate synthesis. The relationships between BCYRN1 and microRNA (miR)‑149, and between miR‑149 and pyruvate kinase M1/2 (PKM2) were measured using a dual‑luciferase reporter assay. Cell proliferation and invasion were analyzed by the Cell Counting kit‑8 assay and the Matrigel invasion assay, respectively. High BCYRN1 expression was observed in NSCLC tissues and cells compared with the corresponding controls. BCYRN1 induced glycolysis and upregulated the expression levels of PKM2 in NSCLC cells. In addition, BCYRN1 regulated miR‑149 expression levels, and miR‑149 inhibitor rescued the effects of si‑BCYRN1 on glucose consumption and lactate production. miR‑149 knockdown significantly enhanced the expression of PKM2. Furthermore, PKM2 inhibition significantly reversed the effects of miR‑149 inhibitor on glucose catabolism and lactate synthesis. Furthermore, PKM2 was involved in NSCLC cell proliferation and invasion, and BCYRN1 knockdown and miR‑149 overexpression inhibited both processes. The present study suggested that BCYRN1 was involved in cell glycolysis, proliferation and invasion during NSCLC via regulating miR‑149 and PKM2.
癌细胞利用有氧糖酵解来维持增殖。长链非编码 RNA 脑细胞质 RNA1（BCYRN1）已被报道在非小细胞肺癌（NSCLC）中作为癌基因发挥作用。本研究探讨了 BCYRN1 在 NSCLC 糖酵解中的作用。使用逆转录-定量 PCR 检测 NSCLC 细胞和组织中的 BCYRN1 表达。通过测量 NSCLC 细胞葡萄糖代谢和乳酸合成来检测 BCYRN1 对有氧糖酵解的影响。使用双荧光素酶报告基因测定测量 BCYRN1 与 microRNA（miR）-149 之间以及 miR-149 与丙酮酸激酶 M1/2（PKM2）之间的关系。通过细胞计数试剂盒-8 测定和 Matrigel 侵袭测定分别分析细胞增殖和侵袭。与相应对照相比，NSCLC 组织和细胞中观察到高 BCYRN1 表达。BCYRN1 诱导 NSCLC 细胞中的糖酵解并上调 PKM2 的表达水平。此外，BCYRN1 调节 miR-149 表达水平，miR-149 抑制剂挽救了 si-BCYRN1 对葡萄糖消耗和乳酸产生的影响。miR-149 敲低显著增强了 PKM2 的表达。此外，PKM2 抑制显著逆转了 miR-149 抑制剂对葡萄糖代谢和乳酸合成的影响。此外，PKM2 参与 NSCLC 细胞增殖和侵袭，BCYRN1 敲低和 miR-149 过表达抑制这两个过程。本研究表明，BCYRN1 通过调节 miR-149 和 PKM2 参与 NSCLC 细胞的糖酵解、增殖和侵袭。
