Department of Gastrointestinal Surgery, Hubei No. 3 People's Hospital of Jianghan University, Wuhan, Hubei, China.
Department of Thyroid and Breast Surgery, Hubei No. 3 People's Hospital of Jianghan University, Wuhan, Hubei, China.
Bioengineered. 2022 May;13(5):13407-13421. doi: 10.1080/21655979.2022.2072629.
Gastric cancer (GC) places a heavy burden on global health, and the information on the molecular mechanism of the progression of GC is still inadequate. Long noncoding RNA (LncRNA) has been confirmed to be widely involved in regulating the progression of GC. Our aim in this study was to explore the role and potential regulatory mechanism of lncRNA BBOX1-AS1 in GC. The expression levels of BBOX1-AS1, miR-361-3p, and MUC13 in GC tissues and cells were evaluated using quantitative real-time polymerase chain reaction and western blotting. The silencer of BBOX1 antisense RNA 1 (BBOX1-AS1) and mucin 13 (MUC13), the mimics and inhibitor of miR-361-3p, and their negative controls were used to alter the expression of these genes. Luciferase reporter, pull-down, and RNA immunoprecipitation assays were performed to verify the correlation between miR-361-3p, BBOX1-AS1, and MUC13. GC cell proliferation, invasion, and apoptosis were detected by cell counting kit-8, transwell, and flow cytometry assays, respectively. An functional experiment was performed to assess the effect of BBOX1-AS1 on GC. The results showed that BBOX1-AS1 was significantly upregulated in GC tissues. Silencing of BBOX1-AS1 inhibited GC cell proliferation and invasion and inhibited tumor growth , whereas it promoted apoptosis. MiR-361-3p was significantly downregulated in GC and counteracted the inhibitory effects of BBOX1-AS1 on GC progression. MUC13, which is targeted by miR-361-3p, is significantly upregulated in GC. MUC13 silencing inhibited GC progression was aborgated by miR-361-3p inhibitor. Collectively, BBOX1-AS1 silencing inhibits GC progression by regulating the miR-361-3p/MUC13 axis, providing a potential therapeutic biomarker for GC.
胃癌（GC）给全球健康带来了沉重负担，而关于 GC 进展的分子机制的信息仍然不足。长链非编码 RNA（lncRNA）已被证实广泛参与调节 GC 的进展。我们在这项研究中的目的是探讨 lncRNA BBOX1-AS1 在 GC 中的作用和潜在调控机制。使用定量实时聚合酶链反应和蛋白质印迹法评估 GC 组织和细胞中 BBOX1-AS1、miR-361-3p 和 MUC13 的表达水平。使用 BBOX1 反义 RNA 1（BBOX1-AS1）和粘蛋白 13（MUC13）的沉默物、miR-361-3p 的模拟物和抑制剂及其阴性对照来改变这些基因的表达。进行荧光素酶报告、下拉和 RNA 免疫沉淀测定以验证 miR-361-3p、BBOX1-AS1 和 MUC13 之间的相关性。通过细胞计数试剂盒-8、Transwell 和流式细胞术检测分别检测 GC 细胞增殖、侵袭和凋亡。进行功能实验以评估 BBOX1-AS1 对 GC 的影响。结果表明，BBOX1-AS1 在 GC 组织中显著上调。沉默 BBOX1-AS1 抑制 GC 细胞增殖和侵袭，抑制肿瘤生长，而促进凋亡。miR-361-3p 在 GC 中显著下调，拮抗 BBOX1-AS1 对 GC 进展的抑制作用。MUC13 是 miR-361-3p 的靶标，在 GC 中显著上调。MUC13 沉默抑制 GC 进展被 miR-361-3p 抑制剂阻断。总之，沉默 BBOX1-AS1 通过调节 miR-361-3p/MUC13 轴抑制 GC 进展，为 GC 提供了一种潜在的治疗生物标志物。
