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AOC4P suppresses viability and invasion and induces apoptosis in NSCLC cells by inhibiting the Wnt/β-catenin pathway.


  • 影响因子:3.43
  • DOI:10.1016/j.cbi.2020.109110
  • 作者列表:"Li F","Rong T","Cao G","Zhai C","Li Q","Gong R","Li G
  • 发表时间:2020-07-01

:Increasing studies have well-documented the involvement of numerous lncRNAs in regulating the malignant phenotypes of various tumors including non-small cell lung cancer (NSCLC) cells. However, up to date, the effects and mechanism of lncRNA amine oxidase, copper containing 4, pseudogene (AOC4P) in NSCLC progression remain undefined. AOC4P expression in NSCLC cells was detected by qRT-PCR. The protein levels of Wnt/β-catenin pathway-related proteins, matrix metallopeptidase (MMP)-2, and MMP-9 were examined by Western blot. The effects of AOC4P or combined with Wnt agonist BML-284 on the malignant phenotypes in NSCLC cells were explored by CCK-8, Transwell invasion assay, flow cytometry analysis and caspase-3/7 activity. AOC4P was lowly expressed in NSCLC samples and cells. Overexpression of AOC4P inhibited viability, the expression of MMP-2 and MMP-9, and invasion of NSCLC cells. Apoptosis and caspase-3/7 activity were suppressed in response to AOC4P overexpression in NSCLC cells. AOC4P overexpression suppressed tumor growth in a xenograft mouse model. Activation of the Wnt/β-catenin pathway by BML-284 abolished the effects of AOC4P overexpression on cell viability, invasion and apoptosis in NSCLC cells. In conclusion, AOC4P overexpression suppresses viability and invasion and induces apoptosis in NSCLC cells via inhibition of the Wnt/β-catenin pathway.


: 越来越多的研究已经充分证明了许多lncrna参与调节各种肿瘤 (包括非小细胞肺癌 (NSCLC) 细胞) 的恶性表型。然而,迄今为止,lncRNA胺氧化酶、含铜 4 、假基因 (AOC4P) 在NSCLC进展中的作用和机制仍未明确。通过qRT-PCR检测NSCLC细胞中的AOC4P表达。通过Western blot检测Wnt/β-catenin通路相关蛋白、基质金属肽酶 (MMP)-2 和MMP-9 的蛋白水平。通过BML-284 、Transwell侵袭检测、流式细胞术分析和caspase-3/7 活性检测,探讨AOC4P或联合Wnt激动剂CCK-8 对NSCLC细胞恶性表型的影响。AOC4P在NSCLC样品和细胞中低表达。过表达AOC4P抑制NSCLC细胞的活力、MMP-2 和MMP-9 的表达和侵袭。凋亡和caspase-3/7 活性在NSCLC细胞中响应于AOC4P过表达而被抑制。AOC4P过表达抑制异种移植小鼠模型中的肿瘤生长。BML-284 Wnt/β-catenin通路的激活消除了AOC4P过表达对NSCLC细胞活力、侵袭和凋亡的影响。总之,AOC4P过表达通过抑制Wnt/β-catenin途径抑制NSCLC细胞的活力和侵袭并诱导细胞凋亡。



作者列表:["Mammana M","Zuin A","Serra E","Bellini A","Rea F"]

METHODS::Pulmonary artery sling is a rare congenital anomaly of the origin and course of the left pulmonary artery. Patients with this condition typically present with respiratory failure in young infancy, and asymptomatic cases are uncommon. We describe the case of an adult patient with a lung adenocarcinoma of the right upper lobe, extending into the hilum and superior mediastinum, and with a previously unknown pulmonary artery sling anomaly. The local invasiveness of the tumor and the peculiar vascular anatomy contributed to a unique surgical scenario, wherein multiple reconstructive procedures were required.

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作者列表:["Hata A","Nakajima T","Matsusaka K","Fukuyo M","Morimoto J","Yamamoto T","Sakairi Y","Rahmutulla B","Ota S","Wada H","Suzuki H","Matsubara H","Yoshino I","Kaneda A"]

METHODS::Patients with idiopathic pulmonary fibrosis (IPF) have higher risk of developing lung cancer, for example, squamous cell carcinoma (SCC), and show poor prognosis, while the molecular basis has not been fully investigated. Here we conducted DNA methylome analysis of lung SCC using 20 SCC samples with/without IPF, and noncancerous lung tissue samples from smokers/nonsmokers, using Infinium HumanMethylation 450K array. SCC was clustered into low- and high-methylation epigenotypes by hierarchical clustering analysis. Genes hypermethylated in SCC significantly included genes targeted by polycomb repressive complex in embryonic stem cells, and genes associated with Gene Ontology terms, for example, "transcription" and "cell adhesion," while genes hypermethylated specifically in high-methylation subgroup significantly included genes associated with "negative regulation of growth." Low-methylation subgroup significantly correlated with IPF (78%, vs. 17% in high-methylation subgroup, p = 0.04), and the correlation was validated by additional Infinium analysis of SCC samples (n = 44 in total), and data from The Cancer Genome Atlas (n = 390). The correlation between low-methylation subgroup and IPF was further validated by quantitative methylation analysis of marker genes commonly hypermethylated in SCC (HOXA2, HOXA9 and PCDHGB6), and markers specifically hypermethylated in high-methylation subgroup (DLEC1, CFTR, MT1M, CRIP3 and ALDH7A1) in 77 SCC cases using pyrosequencing (p = 0.003). Furthermore, low-methylation epigenotype significantly correlated with poorer prognosis among all SCC patients, or among patients without IPF. Multivariate analysis showed that low-methylation epigenotype is an independent predictor of poor prognosis. These may suggest that lung SCC could be stratified into molecular subtypes with distinct prognosis, and low-methylation lung SCC that significantly correlates with IPF shows unfavorable outcome.

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作者列表:["Zhang L","Yang Y","Chai L","Bu H","Yang Y","Huang H","Ran J","Zhu Y","Li L","Chen F","Li W"]

METHODS::The role of Fyn-related kinase (FRK) in malignant tumors remains controversial. Our study investigated the function of FRK in lung cancer. Immunohistochemistry staining and generating a knockout of FRK by CRISPR/Cas9 in H1299 (FRK-KO-H1299) cells were strategies used to explore the role of FRK. Immunohistochemistry staining indicated that FRK expression was elevated in 223 lung cancer tissues compared to 26 distant normal lung tissues. FRK contributed to poor survival status in lung cancer patients and acted as a predictor for poor prognosis of lung cancer. Knockout of FRK by CRISPR/Cas9 markedly inhibited proliferation, invasion, colony formation and epithelial-mesenchymal transition (EMT) process in the lung cancer cell line H1299. Further exploration indicated that FRK-KO damaged the stemness phenotype of H1299 by inhibiting CD44 and CD133 expression. Seahorse detection and a U-13 C flux assay revealed that FRK-KO induced metabolism reprogramming by inhibiting the Warburg effect and changing the energy type in H1299 cells. Epidermal growth factor stimulation recovered the expression of FRK and biological functions, metabolic reprogramming and stemness phenotype of H1299 cells. FRK plays an oncogenic role in lung cancer cells via a novel regulation mechanism of enhancing the stemness of H1299 cells by inducing metabolism reprogramming, which finally promotes EMT and metastasis. Our study also indicates that FRK could be used as a potential therapeutic target for drug development.

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