MicroRNA-582-5p suppresses non-small cell lung cancer cells growth and invasion via downregulating NOTCH1

Liu, Jianghong; Liu, Shengshuo; Deng, Xiaoyan; Rao, Jiaoyu; Huang, Kejie; Xu, Gengrui; Wang, Xiaokang

doi:10.1371/journal.pone.0217652

Cited by 29 publications

(24 citation statements)

References 37 publications

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“…Herein, we focused on the role of miR-582-5p in NSCLC. It was shown that miR-582-5p suppressed the progression of NSCLC via mitogen-activated protein kinase kinase kinase 2 (MAP3K2) [20], and that miR-582-5p restrains the proliferation and invasion of NSCLC cells via Notch homolog 1, translocation-associated (NOTCH1) [21]. In the present study, we found a new regulatory mechanism involving miR-582-5p in NSCLC.…”

Section: Introductionsupporting

confidence: 49%

“…LncRNA XLOC_006390 potentiates the malignancy of cervical cancer cells through miR-331-3p and miR-338-3p sponging [34]. MiR-582-5p serves as a tumor suppressor in many cancers, including hepatocellular carcinoma, colorectal carcinoma, gastric cancer and NSCLC [20,21,[35][36][37]. MiR-582-5p suppresses the proliferation and metastasis of colorectal cancer cells via Ras-related protein Rab27a [36], and impedes the proliferation and motility of NSCLC cells [21].…”

Section: Discussionmentioning

confidence: 99%

“…MiR-582-5p serves as a tumor suppressor in many cancers, including hepatocellular carcinoma, colorectal carcinoma, gastric cancer and NSCLC [20,21,[35][36][37]. MiR-582-5p suppresses the proliferation and metastasis of colorectal cancer cells via Ras-related protein Rab27a [36], and impedes the proliferation and motility of NSCLC cells [21]. MiR-582-5p was found to be a direct target of NEAT1, and functional experiments showed that NEAT1 undermined NSCLC by sponging miR-582-5p.…”

Section: Discussionmentioning

confidence: 99%

“…Studies have reported that lncRNAs could serve as miRNAs sponges to modulate the levels of target miRNAs and matching downstream genes [25]. LncRNA NEAT1-miRNAs interactions were investigated using starBase online software, and miR-582-5p was chosen for the following experiments due to its tumor suppressor role in NSCLC [20,21]. The binding sequence between NEAT1 and miR-582-5p predicted by starBase database is shown in Fig.…”

Section: Neat1 Can Sponge Mir-582-5pmentioning

confidence: 99%

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LncRNA NEAT1 exacerbates non-small cell lung cancer by upregulating EIF4G2 via miR-582-5p sponging

Zhang

Sun

Zou

2020

ARCH BIOL SCI BELGRA

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In this study, we aimed to elucidate the role of long non-coding RNA nuclear enriched abundant transcript 1 (lncRNA NEAT1) in non-small cell lung cancer (NSCLC). Quantitative real-time polymerase chain reaction (qRT-PCR) was employed to detect the abundance of NEAT1, microRNA-582-5p (miR-582-5p) and eukaryotic translation initiation factor 4 gamma 2 (EIF4G2). Proliferation, apoptosis, metastasis and glycolytic metabolism were determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) flow cytometry, transwell assays and fluorescence-based glucose and lactate assay kits. The targets of NEAT1 and miR-582-5p were predicted by the starBase website, and dual-luciferase reporter and RNA immunoprecipitation (RIP) assays were performed to verify these predictions. Western blot analysis was conducted to detect the protein expression of EIF4G2. A xenograft tumor model was built to clarify the role of NEAT1 in vivo. Results showed that NEAT1 interference inhibited proliferation, metastasis and glycolysis, and facilitated the apoptosis of NSCLC cells. MiR-582-5p was a functional target of NEAT1, and the biological influence of NEAT1 intervention on NSCLC cells was alleviated by transfection with anti-miR-582-5p. MiR-582-5p could bind to EIF4G2 messenger RNA (mRNA); it exerted its antitumor role in NSCLC cells by inhibiting EIF4G2. EIF4G2 was regulated by NEAT1/miR-582-5p signaling. NEAT1 accelerated NSCLC tumor growth via the miR-582-5p/EIF4G2 axis in vivo. In conclusion, NEAT1 affected NSCLC by elevating their malignant potential via the miR-582-5p/EIF4G2 axis.Abbreviations: long non-coding RNA (lncRNA); nuclear enriched abundant transcript 1 (NEAT1); non-small cell lung cancer (NSCLC); eukaryotic translation initiation factor 4 gamma (EIF4G); eukaryotic initiation factor 4F (EIF4F) Arch Biol Sci. 2020;72(2):243-252 https://doi.

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Section: Introductionsupporting

confidence: 49%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Neat1 Can Sponge Mir-582-5pmentioning

confidence: 99%

See 2 more Smart Citations

LncRNA NEAT1 exacerbates non-small cell lung cancer by upregulating EIF4G2 via miR-582-5p sponging

Zhang

Sun

Zou

2020

ARCH BIOL SCI BELGRA

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“…Hub genes and their corresponded target miRNAs are presented in Table . Finally, 31 miRNAs, whose functions were correlated with tumor progression (Chang et al, ; Chang et al, ; Chen et al, ; Gao et al, ; Gu et al, ; Han et al, ; He et al, ; Kucuksayan et al, ; Li, Ma, Zhang, Ji, & Jin, ; Li, Ran, et al, ; Li & He, ; Li, Fu, et al, ; Li, Cui, Li, Zhang, & Li, ; Liu et al, ; Liu, Liu, Deng, et al, ; Liu, Liu, & Lu, ; Liu, Liu, Zhang, Tong, & Gan, ; Liu, Miao, et al, ; Luo et al, ; Tang et al, ; Wang et al, ; Wang, Cao, Su, Li, & Yan, ; Wu et al, ; Wu, Mo, Wan, Dan, & Hu, ; Xia, Jing, Li, & Lv, ; Xu et al, ; Zeng et al, ; Zhang, Hao, et al, ; Zhang et al, , ; Zhu et al, ), drug resistance (Bian et al, ; Gao et al, ; Lin, Xie, Lu, Hu, & Chang, ; Pan, Chen, Shen, & Tantai, ; Su et al, ; Xu et al, ; Zhou, Wang, & Feng, ), radiosensitivity (Liu, Li, & Gao, ), recurrence (Sim et al, ) or autophagy (Pan et al, ) in lung cancer, were identified (Table ).…”

Section: Resultsmentioning

confidence: 99%

Common and distinct features of potentially predictive biomarkers in small cell lung carcinoma and large cell neuroendocrine carcinoma of the lung by systematic and integrated analysis

Dong

Liang

Zhai

et al. 2020

Molec Gen & Gen Med

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Background Large‐cell neuroendocrine carcinoma of the lung (LCNEC) and small‐cell lung carcinoma (SCLC) are neuroendocrine neoplasms. However, the underlying mechanisms of common and distinct genetic characteristics between LCNEC and SCLC are currently unclear. Herein, protein expression profiles and possible interactions with miRNAs were provided by integrated bioinformatics analysis, in order to explore core genes associated with tumorigenesis and prognosis in SCLC and LCNEC. Methods http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE1037 gene expression profiles were obtained from the Gene Expression Omnibus (GEO) database. Differentially expressed genes (DEGs) in LCNEC and SCLC, as compared with normal lung tissues, were selected using the GEO2R online analyzer and Venn diagram software. Gene ontology (GO) analysis was performed using Database for Annotation, Visualization and Integrated Discovery. The biological pathway analysis was performed using the FunRich database. Subsequently, a protein–protein interaction (PPI) network of DEGs was generated using Search Tool for the Retrieval of Interacting Genes and displayed via Cytoscape software. The PPI network was analyzed by the Molecular Complex Detection app from Cytoscape, and 16 upregulated hub genes were selected. The Oncomine database was used to detect expression patterns of hub genes for validation. Furthermore, the biological pathways of these 16 hub genes were re‐analyzed, and potential interactions between these genes and miRNAs were explored via FunRich. Results A total of 384 DEGs were identified. A Venn diagram determined 88 common DEGs. The PPI network was constructed with 48 nodes and 221 protein pairs. Among them, 16 hub genes were extracted, 14 of which were upregulated in SCLC samples, as compared with normal lung specimens, and 10 were correlated with the cell cycle pathway. Furthermore, 57 target miRNAs for 8 hub genes were identified, among which 31 miRNAs were correlated with the progression of carcinoma, drug‐resistance, radio‐sensitivity, or autophagy in lung cancer. Conclusion This study provided effective biomarkers and novel therapeutic targets for diagnosis and prognosis of SCLC and LCNEC.

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LncRNA NEAT1 contributes to the acquisition of a tumor like-phenotype induced by PM 2.5 in lung bronchial epithelial cells via HIF-1α activation

Jiang

Hao

Xie

et al. 2021

Environ Sci Pollut Res

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MicroRNA-582-5p suppresses non-small cell lung cancer cells growth and invasion via downregulating NOTCH1

Cited by 29 publications

References 37 publications

LncRNA NEAT1 exacerbates non-small cell lung cancer by upregulating EIF4G2 via miR-582-5p sponging

LncRNA NEAT1 exacerbates non-small cell lung cancer by upregulating EIF4G2 via miR-582-5p sponging

Common and distinct features of potentially predictive biomarkers in small cell lung carcinoma and large cell neuroendocrine carcinoma of the lung by systematic and integrated analysis

LncRNA NEAT1 contributes to the acquisition of a tumor like-phenotype induced by PM 2.5 in lung bronchial epithelial cells via HIF-1α activation

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