Department of Integrated Medicine & General Medicine, Baoji Central Hospital, Baoji City, Shaanxi Province, 721008, China.
Department of Gastroenterology, Xi'an NO.1 Hospital, Xi'an, Shannxi, 710002, China.
Biochem Biophys Res Commun. 2019 May 21;513(1):127-134. doi: 10.1016/j.bbrc.2019.03.140. Epub 2019 Mar 31.
Numerous previous studies have revealed that many long non-coding RNAs (lncRNAs) are upregulated in gastric cancer (GC) and are associated with tumor onset and progression in GC. ADPGK-AS1, a novel lncRNA, has been discovered as an oncogenic lncRNA in pancreatic cancer while its function in GC remains unclear.
The expression of ADPGK-AS1 and miR-3196 was determined by RT-qPCR. The expression of KDM1B was assessed by RT-qPCR and WB. The association between ADPGK-AS1 and overall survival of GC patients was explored using Kaplan-Meier curves. The function of ADPGK-AS1 in GC was examined through CCK-8, EdU, transwell as well as flow cytometry analysis. The interaction of miR-3196 and ADPGK-AS1 or KDM1B was confirmed by RIP, RNA pull down and luciferase reporter assay.Materials and Methods RESULTS: ADPGK-AS1 was increased in GC tissues and cell lines. GC patients with an increased expression of ADPGK-AS1 had a poor prognosis compared to those with a reduced expression. ADPGK-AS1 knockdown led to inhibition of GC cell proliferation and migration. The suppressive effect of ADPGK-AS1 silence on GC progression was abolished by KDM1B upregulation.Results CONCLUSIONS: We unveiled that ADPGK-AS1 could promote GC progression via sponging miR-3196 and therefore upregulating KDM1B, providing a novel prognostic biomarker and therapeutic target for GC patients.
大量先前的研究表明,许多长链非编码 RNA(lncRNA)在胃癌(GC)中上调,并与 GC 中的肿瘤发生和进展相关。ADPGK-AS1 是一种新型 lncRNA,已在胰腺癌中被发现为致癌 lncRNA,但其在 GC 中的功能尚不清楚。
通过 RT-qPCR 测定 ADPGK-AS1 和 miR-3196 的表达。通过 RT-qPCR 和 WB 评估 KDM1B 的表达。使用 Kaplan-Meier 曲线探讨 ADPGK-AS1 与 GC 患者总体生存率的关系。通过 CCK-8、EdU、Transwell 和流式细胞术分析研究 ADPGK-AS1 在 GC 中的功能。通过 RIP、RNA 下拉和荧光素酶报告基因测定证实 miR-3196 与 ADPGK-AS1 或 KDM1B 的相互作用。
ADPGK-AS1 在 GC 组织和细胞系中增加。与表达减少的患者相比,表达增加的 GC 患者预后较差。ADPGK-AS1 敲低导致 GC 细胞增殖和迁移受到抑制。KDM1B 上调可消除 ADPGK-AS1 沉默对 GC 进展的抑制作用。
我们揭示了 ADPGK-AS1 可以通过海绵 miR-3196 促进 GC 进展,从而上调 KDM1B,为 GC 患者提供了一种新的预后生物标志物和治疗靶点。