Long non-coding RNA TP73-AS1 promotes pancreatic cancer growth and metastasis through miRNA-128-3p/GOLM1 axis.
Long non-coding RNA TP73-AS1 promotes pancreatic cancer growth and metastasis through miRNA-128-3p/GOLM1 axis.
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DOI：
10.3748/wjg.v27.i17.1993
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发表时间：
2021-05-07
影响因子：
4.3
通讯作者：
Qiu ZJ
中科院分区：
文献类型：
--
作者：
Wang B;Sun X;Huang KJ;Zhou LS;Qiu ZJ
先前的研究表明，长非编码 RNA (lncRNA) TP73-AS1 在多种癌症中显着上调。然而，TP73-AS1在胰腺癌（PC）中的生物学作用和临床意义仍不清楚。 探讨TP73-AS1在PC生长和转移中的作用。采用实时定量聚合酶链式反应检测PC组织和细胞中lncRNA TP73-AS1、miR-128-3p和GOLM1的表达。使用生物信息学预测软件ENCORI预测miR-128-3p的假定结合位点。 TP73-AS1 和 miR-128-3p 在细胞增殖、迁移和侵袭能力中的调节作用通过 Cell Counting Kit-8、伤口愈合和 Transwell 实验以及流式细胞术和 Western blot 分析进行了验证。通过生物信息学预测、荧光素酶测定和蛋白质印迹探索 TP73-AS1、miR-128-3p 和 GOLM1 之间的相互作用。 PC组织和细胞中TP73-AS1和miRNA-128-3p的表达失调。 TP73-AS1 高表达与不良预后相关。 TP73-AS1 沉默可抑制体外 PC 细胞增殖、迁移和侵袭，并抑制体内肿瘤生长。从机制上讲，TP73-AS1 被验证可通过竞争性结合 miR-128-3p 上调 GOLM1 来促进 PC 进展。 我们的结果表明，TP73-AS1 通过调节 miR-128-3p/GOLM1 轴促进 PC 进展，这可能为 PC 患者提供潜在的治疗策略。
Previous studies have suggested that long non-coding RNAs (lncRNA) TP73-AS1 is significantly upregulated in several cancers. However, the biological role and clinical significance of TP73-AS1 in pancreatic cancer (PC) remain unclear. To investigate the role of TP73-AS1 in the growth and metastasis of PC. The expression of lncRNA TP73-AS1, miR-128-3p, and GOLM1 in PC tissues and cells was detected by quantitative real-time polymerase chain reaction. The bioinformatics prediction software ENCORI was used to predict the putative binding sites of miR-128-3p. The regulatory roles of TP73-AS1 and miR-128-3p in cell proliferation, migration, and invasion abilities were verified by Cell Counting Kit-8, wound-healing, and transwell assays, as well as flow cytometry and Western blot analysis. The interactions among TP73-AS1, miR-128-3p, and GOLM1 were explored by bioinformatics prediction, luciferase assay, and Western blot. The expression of TP73-AS1 and miRNA-128-3p was dysregulated in PC tissues and cells. High TP73-AS1 expression was correlated with a poor prognosis. TP73-AS1 silencing inhibited PC cell proliferation, migration, and invasion in vitro as well as suppressed tumor growth in vivo. Mechanistically, TP73-AS1 was validated to promote PC progression through GOLM1 upregulation by competitively binding to miR-128-3p. Our results demonstrated that TP73-AS1 promotes PC progression by regulating the miR-128-3p/GOLM1 axis, which might provide a potential treatment strategy for patients with PC.
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