Long intergenic non-protein coding RNA 319 aggravates lung adenocarcinoma carcinogenesis by modulating miR-450b-5p/EZH2

Zhang, Zeng-Wang; Chen, Jiajun; Xia, Shihui; Zhao, Hua; Jy, Yang; Zhang, Hao; He, Bin; Jiao, Jun; Zhan, Bo-Tao; Sun, Chengcao

doi:10.1016/j.gene.2018.01.096

Cited by 58 publications

(44 citation statements)

References 39 publications

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“…U3 is upregulated with age until the sixth decade of life and is a regulator of 18 s rRNA folding during ribosome biogenesis (Dutca, Gallagher, & Baserga, ). In contrast, LINC00319 is down‐regulated with age and promotes tumor growth via transcriptional silencing (Zhang et al, ). Given the emerging evidence that lncRNAs help direct mTOR specificity in vitro (Chen et al, ; Li et al, ), this suggests that our age‐regulated lncRNAs can fine‐tune the regulation of longevity‐related proteins.…”

Section: Discussionmentioning

confidence: 99%

Longevity‐related molecular pathways are subject to midlife “switch” in humans

et al. 2019

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Emerging evidence indicates that molecular aging may follow nonlinear or discontinuous trajectories. Whether this occurs in human neuromuscular tissue, particularly for the noncoding transcriptome, and independent of metabolic and aerobic capacities, is unknown. Applying our novel RNA method to quantify tissue coding and long noncoding RNA (lncRNA), we identified ~800 transcripts tracking with age up to ~60 years in human muscle and brain. In silico analysis demonstrated that this temporary linear “signature” was regulated by drugs, which reduce mortality or extend life span in model organisms, including 24 inhibitors of the IGF‐1/PI3K/mTOR pathway that mimicked, and 5 activators that opposed, the signature. We profiled Rapamycin in nondividing primary human myotubes (n = 32 HTA 2.0 arrays) and determined the transcript signature for reactive oxygen species in neurons, confirming that our age signature was largely regulated in the “pro‐longevity” direction. Quantitative network modeling demonstrated that age‐regulated ncRNA equaled the contribution of protein‐coding RNA within structures, but tended to have a lower heritability, implying lncRNA may better reflect environmental influences. Genes ECSIT, UNC13, and SKAP2 contributed to a network that did not respond to Rapamycin, and was associated with “neuron apoptotic processes” in protein–protein interaction analysis (FDR = 2.4%). ECSIT links inflammation with the continued age‐related downwards trajectory of mitochondrial complex I gene expression (FDR < 0.01%), implying that sustained inhibition of ECSIT may be maladaptive. The present observations link, for the first time, model organism longevity programs with the endogenous but temporary genome‐wide responses to aging in humans, revealing a pattern that may ultimately underpin personalized rates of health span.

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Section: Discussionmentioning

confidence: 99%

Longevity‐related molecular pathways are subject to midlife “switch” in humans

et al. 2019

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“…[10][11][12] LINC00319, a novel cancer-related lncRNA, is transcribed from an intergenic region of chromosome 21. 14 Nonetheless, the biological role of LINC00319 in CSCC remains poorly understood. 14 Nonetheless, the biological role of LINC00319 in CSCC remains poorly understood.…”

Section: Introductionmentioning

confidence: 99%

Upregulation of LINC00319 indicates a poor prognosis and promotes cell proliferation and invasion in cutaneous squamous cell carcinoma

Liao

Duan

et al. 2018

J of Cellular Biochemistry

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Cutaneous squamous cell carcinoma (CSCC), an epidermal keratinocyte-derived skin tumor, is one of the most leading causes of cancer-associated morbidity and mortality worldwide. Long noncoding RNAs have emerged as key regulators of tumor development and progression. Recent studies have identified LINC00319, a long intergenic noncoding RNA, as an oncogene in lung cancer. However, the biological role of LINC00319 in CSCC remains largely unknown. The current study aimed to explore the role of LINC00319 in CSCC and uncover the molecular mechanisms. In current study, we found that LINC00319 was significantly upregulated in both CSCC tissues and cell lines. Besides, the χ test showed that increased expression of LINC00319 was associated with larger tumor size, advanced TNM stage, and lymphovascular invasion. Gain-of-function and loss-of-function approaches were applied to investigate the effects of LINC00319 on CSCC cells. Functional studies demonstrated that LINC00319 promoted CSCC cell proliferation, accelerated cell cycle progression, facilitated cell migration and invasion, and inhibited cell apoptosis. Mechanistic studies revealed that LINC00319 exerts its oncogenic functions in CSCC via miR-1207-5p-mediated regulation of cyclin-dependent kinase 3. Taken together, upregulation of LINC00319 implies a potential link with poor prognosis and reflects CSCC progression. Collectively, this study may provide some evidence for LINC00319 as a candidate target in CSCC treatment.

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“…The correlation between lncRNAs and LAD has not been definitively determined. Several lncRNAs have been proposed as oncogenic in LAD, including LINC00707, LINC00319, and lncRNA MIR31HG . However, whether lncRNAs are related to the occurrence of LAD, and whether differentially expressed lncRNAs could be considered significant with the presence or absence of lymphatic metastasis has not yet been determined.…”

Section: Discussionmentioning

confidence: 99%

“…Thoracic Cancer 9 (2018) 1312-1322 LINC00319, and lncRNA MIR31HG. [24][25][26] However, whether lncRNAs are related to the occurrence of LAD, and whether differentially expressed lncRNAs could be considered significant with the presence or absence of lymphatic metastasis has not yet been determined.…”

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confidence: 99%

Microarray expression profile of long non‐coding RNAs in human lung adenocarcinoma

et al. 2018

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BackgroundLong non‐coding RNAs (lncRNAs) participate in many biological dynamics and play significant roles in gene regulation. LncRNA expression is altered in many cancers; however, the expressions and functions of lncRNA genes in lung adenocarcinoma (LAD) remain unknown.MethodsLncRNA and messenger RNA (mRNA) expression in LAD without lymphatic metastasis versus paired adjacent non‐tumor (ANT) lung tissues and LAD with versus without lymphatic metastasis were analyzed using Human LncRNA Arraystar V3.0. The expression levels of four downregulated and four upregulated lncRNAs were verified using quantitative real‐time PCR in cells and tissue specimens.ResultsIn this study, 949 lncRNAs and 681 mRNAs had differential expression in LAD without lymphatic metastasis compared to ANT lung tissues, while 2740 lncRNAs and 1714 mRNAs were differentially expressed in LAD with lymphatic metastasis compared to LAD without lymphatic metastasis. The expression patterns of selected lncRNAs (LINC00113, AC005009.1, ARHGAP22‐IT1, AC009411.1, SRGAP3‐AS2, EGFEM1P, FAM66E, and HLA‐F‐AS1) were consistent with microarray data. Differentially expressed mRNA genes were enriched in crucial Gene Ontology terms and pathways.ConclusionOur results revealed differentially expressed lncRNAs in LAD, suggesting lncRNAs may be potential indicators for LAD diagnosis and therapy.

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Long intergenic non-protein coding RNA 319 aggravates lung adenocarcinoma carcinogenesis by modulating miR-450b-5p/EZH2

Cited by 58 publications

References 39 publications

Longevity‐related molecular pathways are subject to midlife “switch” in humans

Longevity‐related molecular pathways are subject to midlife “switch” in humans

Upregulation of LINC00319 indicates a poor prognosis and promotes cell proliferation and invasion in cutaneous squamous cell carcinoma

Microarray expression profile of long non‐coding RNAs in human lung adenocarcinoma

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