MiR-216a-5p has opposite effects on tumorigenesis and progression in the context of different tumors, acting as either a tumor suppressor or an oncogene. However, the expression and function of miR-216a-5p in pancreatic cancer (PC) is not well characterized./nIn this study, we found miR-216a-5p was significantly downregulated in PC tissues and cell lines, which showed a negative correlation with peripancreatic lymph, perineural invasion and TNM stage of PCs patients. We made use of functional assays to reveal that miR-216a-5p inhibited growth and migration of PC cells in vitro and in vivo. Then, by employing the bioinformatics analysis and luciferase reporter assay, we demonstrated TPT1 was a potential target of miR-216a-5p, which contributes to tumor malignance by mediating mTORC1 pathway-associated autophagy. Furthermore, bioinformatics analysis and RNA pulldown confirmed that miR-216a-5p was mediated by LINC01133, which sponge miR-216a-5p, as a competing endogenous RNA (ceRNA). Collectively, our study revealed an important role of LINC01133/miR-216a-5p/TPT1 axis in the genesis and progression of PCs, which provides potential biomarkers for clinical diagnosis and therapy of PCs.

中文翻译：

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MiR-216a-5p 通过靶向 TPT1/mTORC1 并由 LINC01133 介导抑制胰腺癌的肿瘤发生。


MiR-216a-5p 在不同肿瘤的背景下对肿瘤发生和进展具有相反的作用，充当肿瘤抑制基因或癌基因。然而，miR-216a-5p在胰腺癌（PC）中的表达和功能尚未得到很好的表征。/n在本研究中，我们发现miR-216a-5p在PC组织和细胞系中显着下调，呈负相关PCs 患者的胰周淋巴、神经周围浸润和 TNM 分期。我们利用功能测定揭示了 miR-216a-5p在体外和体内抑制 PC 细胞的生长和迁移。然后，通过生物信息学分析和荧光素酶报告基因检测，我们证明TPT1是miR-216a-5p的潜在靶标，miR-216a-5p通过介导mTORC1通路相关的自噬而导致肿瘤恶性。此外，生物信息学分析和 RNA Pulldown 证实 miR-216a-5p 由 LINC01133 介导，LINC01133 将 miR-216a-5p 作为竞争性内源 RNA (ceRNA) 吸收。总的来说，我们的研究揭示了LINC01133/miR-216a-5p/TPT1轴在PC发生和进展中的重要作用，这为PC的临床诊断和治疗提供了潜在的生物标志物。