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PNO1, which is negatively regulated by miR-340-5p, promotes lung adenocarcinoma progression through Notch signaling pathway.
Oncogenesis ( IF 5.9 ) Pub Date : 2020-06-01 , DOI: 10.1038/s41389-020-0241-0
Dongming Liu 1, 2, 3 , Li Lin 3, 4 , Yajie Wang 3, 4 , Lu Chen 1, 2, 3 , Yuchao He 1, 3 , Yi Luo 1, 3 , Lisha Qi 3, 5 , Yan Guo 3, 6 , Liwei Chen 1, 3 , Zhiqiang Han 1, 2, 3 , Guangtao Li 1, 2, 3 , Qiang Li 2, 3 , Zhiyong Liu 1, 3 , Peng Chen 3, 4 , Hua Guo 1, 3
Affiliation  

Many studies have shown that the hyperactivation of ribosome biogenesis plays essential roles in the initiation and progression of cancers. As a ribosome assembly factor, PNO1 plays an important role in ribosome biogenesis. However, little is known about the expression and function of PNO1 in human tumors. In our present study, we aimed to explore the functional roles and the underlying molecular mechanisms of PNO1 in human lung adenocarcinoma (LUAD). Both bioinformatics databases and tumor tissues demonstrated that the expression of PNO1 in LUAD tissues was higher than that in adjacent tissues and predicted poor survival in LUAD patients. In vitro and in vivo assays suggested that downregulation of PNO1 expression suppressed LUAD cell proliferation and invasion. Further studies found that miR-340-5p depressed PNO1 expression via direct binding to the 3′ untranslated region (UTR) of PNO1. PNO1 expression was negatively correlated with miR-340-5p expression in LUAD cells and tissue samples. Moreover, upregulation or downregulation of miR-340-5p expression reversed the effects of PNO1 inhibition and overexpression, respectively. Meanwhile, downregulation of PNO1 inhibited Notch signaling pathway which modulated epithelial mesenchymal transition (EMT). These results indicate that PNO1, negatively regulated by miR-340-5p, played an important role in LUAD progression via Notch signaling pathway. The miR-340-5p/PNO1/Notch axis might be a potential target for individualized and precise treatment of LUAD patients in the future.



中文翻译:

PNO1 受 miR-340-5p 负调控,通过 Notch 信号通路促进肺腺癌进展。

许多研究表明,核糖体生物发生的过度激活在癌症的发生和发展中起着至关重要的作用。作为核糖体组装因子,PNO1在核糖体生物发生中起重要作用。然而,关于 PNO1 在人类肿瘤中的表达和功能知之甚少。在我们目前的研究中,我们旨在探索 PNO1 在人肺腺癌 (LUAD) 中的功能作用和潜在的分子机制。生物信息学数据库和肿瘤组织均表明,LUAD 组织中 PNO1 的表达高于邻近组织,预示着 LUAD 患者的生存率较差。体外和体内试验表明,PNO1 表达的下调抑制了 LUAD 细胞的增殖和侵袭。进一步的研究发现,miR-340-5p 通过直接结合 PNO1 的 3' 非翻译区 (UTR) 来抑制 PNO1 的表达。PNO1 表达与 LUAD 细胞和组织样本中的 miR-340-5p 表达呈负相关。此外,miR-340-5p 表达的上调或下调分别逆转了 PNO1 抑制和过表达的影响。同时,PNO1的下调抑制了调节上皮间质转化(EMT)的Notch信号通路。这些结果表明,由 miR-340-5p 负调控的 PNO1 通过 Notch 信号通路在 LUAD 进展中发挥重要作用。miR-340-5p/PNO1/Notch轴可能是未来LUAD患者个体化和精准治疗的潜在靶点。PNO1 表达与 LUAD 细胞和组织样本中的 miR-340-5p 表达呈负相关。此外,miR-340-5p 表达的上调或下调分别逆转了 PNO1 抑制和过表达的影响。同时,PNO1的下调抑制了调节上皮间质转化(EMT)的Notch信号通路。这些结果表明,由 miR-340-5p 负调控的 PNO1 通过 Notch 信号通路在 LUAD 进展中发挥重要作用。miR-340-5p/PNO1/Notch轴可能是未来LUAD患者个体化和精准治疗的潜在靶点。PNO1 表达与 LUAD 细胞和组织样本中的 miR-340-5p 表达呈负相关。此外,miR-340-5p 表达的上调或下调分别逆转了 PNO1 抑制和过表达的影响。同时,PNO1的下调抑制了调节上皮间质转化(EMT)的Notch信号通路。这些结果表明,由 miR-340-5p 负调控的 PNO1 通过 Notch 信号通路在 LUAD 进展中发挥重要作用。miR-340-5p/PNO1/Notch轴可能是未来LUAD患者个体化和精准治疗的潜在靶点。PNO1的下调抑制了调节上皮间质转化(EMT)的Notch信号通路。这些结果表明,由 miR-340-5p 负调控的 PNO1 通过 Notch 信号通路在 LUAD 进展中发挥重要作用。miR-340-5p/PNO1/Notch轴可能是未来LUAD患者个体化和精准治疗的潜在靶点。PNO1的下调抑制了调节上皮间质转化(EMT)的Notch信号通路。这些结果表明,由 miR-340-5p 负调控的 PNO1 通过 Notch 信号通路在 LUAD 进展中发挥重要作用。miR-340-5p/PNO1/Notch轴可能是未来LUAD患者个体化和精准治疗的潜在靶点。

更新日期:2020-06-01
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