Guo Shengcong, Mao Zejun, Zhang Guodong, Xu Botao, He Xiangfeng
Department of Cardiothoracic Surgery, Zhuji People's Hospital, Zhuji, China.
Department of Cardiothoracic Surgery, Zhuji Hospital Affiliated to Shaoxing University, Zhuji, China.
Transl Cancer Res. 2022 Mar;11(3):519-529. doi: 10.21037/tcr-22-195.
Non-small cell lung carcinoma (NSCLC) is a highly malignant tumor with a poor prognosis worldwide. Some studies have demonstrated that circular pleiotrophin (circPTN) plays critical roles in tumorigenesis and tumor development. However, little is known about the role of circPTN in NSCLC.
The circPTN expression in human NSCLC tissues was measured via quantitative real-time polymerase chain reaction (qRT-PCR). The function and potential mechanisms of circPTN in NSCLC angiogenesis were also investigated. We aimed to explore the function and potential mechanisms and clinical significance of circPTN in NSCLC.
We first found that circPTN was markedly upregulated in NSCLC tissues. A higher circPTN level was closely associated with angiogenesis and significantly shorter overall survival in patients with NSCLC. We then found that circPTN promoted angiogenesis in NSCLC. More importantly, we found that circPTN facilitated angiogenesis by regulating the expression of LYRM5 in NSCLC. Mechanistically, LYRM5 could be a direct target of microRNA-595 (miR-595). Additionally, we demonstrated that circPTN upregulated LYRM5 expression by sponging miR-595, which promoted NSCLC angiogenesis in NSCLC.
We found that circPTN serves as a competing endogenous ribonucleic acid that promotes angiogenesis via the miR-595/LYRM5 signaling pathway in NSCLC. Targeting circPTN might be a promising new therapeutic strategy for NSCLC.
非小细胞肺癌(NSCLC)是一种高度恶性的肿瘤,在全球范围内预后较差。一些研究表明,环状多效生长因子(circPTN)在肿瘤发生和肿瘤发展中起关键作用。然而,关于circPTN在NSCLC中的作用知之甚少。
通过定量实时聚合酶链反应(qRT-PCR)检测人NSCLC组织中circPTN的表达。还研究了circPTN在NSCLC血管生成中的功能和潜在机制。我们旨在探讨circPTN在NSCLC中的功能、潜在机制及临床意义。
我们首先发现circPTN在NSCLC组织中显著上调。circPTN水平较高与血管生成密切相关,且与NSCLC患者的总生存期显著缩短有关。然后我们发现circPTN促进NSCLC中的血管生成。更重要的是,我们发现circPTN通过调节NSCLC中LYRM5的表达促进血管生成。机制上,LYRM5可能是微小RNA-595(miR-595)的直接靶标。此外,我们证明circPTN通过海绵吸附miR-595上调LYRM5表达,从而促进NSCLC中的血管生成。
我们发现circPTN作为一种竞争性内源性核糖核酸通过miR-595/LYRM5信号通路促进NSCLC中的血管生成。靶向circPTN可能是NSCLC一种有前景的新治疗策略。