Comprehensive analysis of differentially expressed long non‑coding RNAs in non‑small cell lung cancer

Zhou, Wenyong; Liu, Tao; Saren, Gaowa; Liao, Li; Fang, Wentao; Zhao, Heng

doi:10.3892/ol.2019.10414

Cited by 20 publications

(25 citation statements)

References 40 publications

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“…In vivo experiments also discovered that LINC00667 knockdown or miR-143-3p overexpression could decrease the expression of RRM2 and proliferation-related genes, therefore inhibiting the growth of tumor. Recently Zhou et al reported that LINC00667 was one of seven lincRNAs involved in the progression of NSCLS, which is consistent with our current findings 33…”

Section: Discussionsupporting

confidence: 93%

<p>RRM2 Regulated By LINC00667/miR-143-3p Signal Is Responsible For Non-Small Cell Lung Cancer Cell Progression</p>

Yang

Sen-sen

Cao

et al. 2019

OTT

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Background: Non-small cell lung cancer (NSCLC) is a common and fatal cancer worldwide with a very low 5-year overall survival rate. Ribonucleotide reductase M2 subunit (RRM2), a small subunit of the ribonucleotide reductase complex, has been found to be an oncogenic role in a variety of tumors including NSCLC. However, the regulatory mechanism of RRM2 in NSCLC is not clear. Increasing evidence suggests that non-coding RNAs (ncRNAs) including miRNAs and lincRNAs may promote or inhibit tumor initiation and development through regulating the expression of oncogenic genes. It is interesting to find ncRNAs which play important role in regulating RRM2 expression. Materials and methods: The expression levels of RRM2, LINC0066 and miR-143-3p in NSCLC tumor tissues and cell lines were detected using qRT-PCR. The regulatory relationships among RRM2, LINC0066 and miR-143-3p were predicted using database analysis and verified by luciferase reporter assay and RIP analysis. The proliferation ability of NSCLC cells was assessed using CCK8 and colony formation assays. The expression of related proteins was determined by Western blot. In vivo effect of RRM2, LINC0066 and miR-143-3p to NSCLC were detected through xenograft experiments. Results: In this study, we found RRM2 was upregulated in NSCLC tumor and cell lines, and the aberrant upregulation predicted a poor prognosis. Then, we predicted and confirmed that RRM2 was negatively regulated by miR-143-3p. Further study implied that LINC00667 acted as a ceRNA by sponging miR-143-3p and regulated RRM2 expression indirectly. Moreover, we found that the growth of NSCLC was regulated by LINC00667/miR-143-3p/RRM2 signal pathway both in vitro and in vivo. LINC00667 and RRM2 promoted the tumor growth while miR-143-3p inhibited it. Conclusion: Our study revealed a LINC00667/miR-143-3p/RRM2 signal pathway that played an important role in the progress of NSCLC, which might be potential therapeutic targets for NSCLC.

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Section: Discussionsupporting

confidence: 93%

<p>RRM2 Regulated By LINC00667/miR-143-3p Signal Is Responsible For Non-Small Cell Lung Cancer Cell Progression</p>

Yang

Sen-sen

Cao

et al. 2019

OTT

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“…In our study, only one lncRNA, GVINP1, was found to be associated with the overall survival in luminal BC. The lncRNA GVINP1 can bind with guanosine triphosphate selectively and noncovalently, and it has been found to be an independent prognostic marker for lung adenocarcinoma (LUAD) and NSCLC patients ( Sui and Yang, 2019 ; Zhou et al, 2019 ). Our study also indicated that high expression of GVINP1 could compete with the downregulated miRNA hsa-miR-149-5p to regulate the expression of target genes, including several novel survival-associated genes such as CCDC69, DOCK2, IKZF1, JCHAIN, and NCKAP1L involved in the ceRNA network.…”

Section: Discussionmentioning

confidence: 99%

Identification of Tumor Microenvironment-Related Prognostic Biomarkers in Luminal Breast Cancer

et al. 2020

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Background: The tumor microenvironment (TME) has been reported to have significant value in the diagnosis and prognosis of cancers. This study aimed to identify key biomarkers in the TME of luminal breast cancer (BC).Methods: We obtained immune scores (ISs) and stromal scores (SSs) for The Cancer Genome Atlas (TCGA) luminal BC cohort from the online ESTIMATE (Estimation of STromal and Immune cells in MAlignant Tumor tissues using Expression data) portal. The relationships between ISs and SSs and the overall survival of luminal BC patients were assessed by the Kaplan-Meier method. The differentially expressed messenger RNAs (DEmRNAs) related to the ISs and SSs were subjected to functional enrichment analysis. Additionally, a competing endogenous RNA (ceRNA) network was constructed with differentially expressed microRNAs (DEmiRNAs) and long noncoding RNAs (DElncRNAs). Furthermore, a protein–protein interaction (PPI) network was established to analyze the DEmRNAs in the ceRNA network. Then, survival analysis of biomarkers involved in the ceRNA network was carried out to explore their prognostic value. Finally, these biomarkers were validated using the luminal BC dataset from the Gene Expression Omnibus (GEO) database.Results: The results showed that ISs were significantly associated with longer survival times of luminal BC patients. Functional enrichment analysis showed that the DEmRNAs were mainly associated with immune response, antigen binding, and the extracellular region. In the PPI network, the top 10 DEmRNAs were identified as hub genes that affected the TME of luminal BC. Finally, two DEmiRNAs, two DElncRNAs, and 17 DEmRNAs of the ceRNA network associated with the TME were shown to have prognostic value. Subsequently, the expression of 15 prognostic biomarkers was validated in one additional dataset (GSE81002). In particular, one lncRNA (GVINP1) and five mRNAs (CCDC69, DOCK2, IKZF1, JCHAIN, and NCKAP1L) were novel biomarkers.Conclusions: Our studies demonstrated that ISs were associated with the survival of luminal BC patients, and a set of novel biomarkers that might play a prognostic role in the TME of luminal BC was identified.

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“…The localization of lncRNAs largely reflects their function, and they can interact with chromatin, protein, and RNA to regulate all stages of gene expression and influence important signaling cascades [9]. Although normally tightly regulated, large-scale analyses revealed that lncRNAs are commonly dysregulated in NSCLC [36]. Many lncRNAs are upregulated and function as oncogenes to enhance NSCLC proliferation, survival, invasion, migration, EMT, and metastasis.…”

Section: Discussionmentioning

confidence: 99%

“…Many large-scale analyses investigated differentially expressed lncRNAs in NSCLC [35,36]. As shown in Table 1, most upregulated lncRNAs in NSCLC function as oncogenes, whereas less commonly downregulated lncRNAs function as tumor suppressors (Table 2).…”

Section: Lncrna Dysregulation In Nsclcmentioning

confidence: 99%

LncRNAs in Non-Small-Cell Lung Cancer

Ginn

Shi

Montagna

et al. 2020

ncRNA

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Lung cancer is associated with a high mortality, with around 1.8 million deaths worldwide in 2018. Non-small-cell lung cancer (NSCLC) accounts for around 85% of cases and, despite improvement in the management of NSCLC, most patients are diagnosed at advanced stage and the five-year survival remains around 15%. This highlights a need to identify novel ways to treat the disease to reduce the burden of NSCLC. Long non-coding RNAs (lncRNAs) are non-coding RNA molecules longer than 200 nucleotides in length which play important roles in gene expression and signaling pathways. Recently, lncRNAs were implicated in cancer, where their expression is dysregulated resulting in aberrant functions. LncRNAs were shown to function as both tumor suppressors and oncogenes in a variety of cancer types. Although there are a few well characterized lncRNAs in NSCLC, many lncRNAs remain un-characterized and their mechanisms of action largely unknown. LncRNAs have success as therapies in neurodegenerative diseases, and having a detailed understanding of their function in NSCLC may guide novel therapeutic approaches and strategies. This review discusses the role of lncRNAs in NSCLC tumorigenesis, highlighting their mechanisms of action and their clinical potential.

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Comprehensive analysis of differentially expressed long non‑coding RNAs in non‑small cell lung cancer

Cited by 20 publications

References 40 publications

<p>RRM2 Regulated By LINC00667/miR-143-3p Signal Is Responsible For Non-Small Cell Lung Cancer Cell Progression</p>

<p>RRM2 Regulated By LINC00667/miR-143-3p Signal Is Responsible For Non-Small Cell Lung Cancer Cell Progression</p>

Identification of Tumor Microenvironment-Related Prognostic Biomarkers in Luminal Breast Cancer

LncRNAs in Non-Small-Cell Lung Cancer

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