Long Noncoding RNA MRPL39 Inhibits Gastric Cancer Proliferation and Progression by Directly Targeting miR-130

Yu, Ming; Zhao, Na; Shen, Haibin; Wang, Haiming

doi:10.1089/gtmb.2018.0151

Cited by 15 publications

(15 citation statements)

References 36 publications

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“…The colony formation assay also confirmed these results since less colonies were formed by the cells overexpressing LINC02381. This miRNA-mediated tumor-suppressive effect has also been reported for SNHG12 (44), MRPL39 (45), and GAS5 (46) lncRNAs, which modulate signaling pathways in gastric cancer by sponging different miRNAs.…”

Section: Discussionsupporting

confidence: 60%

RETRACTED: Long Noncoding RNA LOC400043 (LINC02381) Inhibits Gastric Cancer Progression Through Regulating Wnt Signaling Pathway

Jafarzadeh

Soltani

2020

Front. Oncol.

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Gastric cancer is one of the common causes of cancer mortality worldwide, with a low survival rate for the affected people. Recent studies have revealed the key role of long non-coding RNAs (lncRNAs) in the development and progression of many cancers, including gastric cancer. Looking for the potential molecular regulators of gastric cancer incidence and progression, LINC02381 was identified as a downregulated lncRNA in gastric cancer tissues by analysis of available microarray and RNA-seq data and RT-qPCR confirmed this differential expression. MiR-21, miR-590, and miR-27a miRNAs were predicted to be sponged by LINC02381, and dual luciferase assay verified LINC02381 as a competitive endogenous RNA (CeRNA), which binds to them. Furthermore, we found that increased expression of LINC02381 attenuates Wnt pathway activity. Also, functional analysis indicates that LINC02381 arrests cell cycle, increases apoptosis and caspase activity, and reduces cell survival and proliferation rate of the human gastric cancer cell lines AGS and MKN45. Moreover, EMT analysis showed that LINC02381 is involved in gastric cancer progression and inhibits metastasis. Overall, this work for the first time introduces LINC02381 as a CeRNA involved in gastric cancer and provides novel insight into the molecular pathogenesis of gastric cancer.

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Section: Discussionsupporting

confidence: 60%

RETRACTED: Long Noncoding RNA LOC400043 (LINC02381) Inhibits Gastric Cancer Progression Through Regulating Wnt Signaling Pathway

Jafarzadeh

Soltani

2020

Front. Oncol.

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“…In pathway enrichment analysis for up regulated genes, genes such as RPLP0 [80] and MRPS30 [81] were associated with pathogenesis of many cancer types such as gastric cancer and breast cancer, but these genes may be responsible for advancement of GBM. Inactivation of tumor suppressor genes such as RPS7 [82], MRPL39 [83], MRPS23 [84], ME2 [85], and NDUFB9 [86] were diagnosed with the development of many cancer types such as colorectal cancer, gastric cancer, breast cancer, and pancreatic cancer, but loss of these genes may be responsible for the development of GBM. RPS24 [87] was linked with the proliferation of colon cancer cells, but this gene may be linked with the proliferation of GBM cells.…”

Section: Discussionmentioning

confidence: 99%

Identification of Crucial Candidate Genes and Pathways in Glioblastoma Multiform by Bioinformatics Analysis

Alshabi

Vastrad²,

Shaikh

et al. 2019

Biomolecules

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The present study aimed to investigate the molecular mechanisms underlying glioblastoma multiform (GBM) and its biomarkers. The differentially expressed genes (DEGs) were diagnosed using the limma software package. The ToppGene (ToppFun) was used to perform pathway and Gene Ontology (GO) enrichment analysis of the DEGs. Protein-protein interaction (PPI) networks, extracted modules, miRNA-target genes regulatory network and TF-target genes regulatory network were used to obtain insight into the actions of DEGs. Survival analysis for DEGs was carried out. A total of 590 DEGs, including 243 up regulated and 347 down regulated genes, were diagnosed between scrambled shRNA expression and Lin7A knock down. The up-regulated genes were enriched in ribosome, mitochondrial translation termination, translation, and peptide biosynthetic process. The down-regulated genes were enriched in focal adhesion, VEGFR3 signaling in lymphatic endothelium, extracellular matrix organization, and extracellular matrix. The current study screened the genes in the PPI network, extracted modules, miRNA-target genes regulatory network, and TF-target genes regulatory network with higher degrees as hub genes, which included NPM1, CUL4A, YIPF1, SHC1, AKT1, VLDLR, RPL14, P3H2, DTNA, FAM126B, RPL34, and MYL5. Survival analysis indicated that the high expression of RPL36A and MRPL35 were predicting longer survival of GBM, while high expression of AP1S1 and AKAP12 were predicting shorter survival of GBM. High expression of RPL36A and AP1S1 were associated with pathogenesis of GBM, while low expression of ALPL was associated with pathogenesis of GBM. In conclusion, the current study diagnosed DEGs between scrambled shRNA expression and Lin7A knock down samples, which could improve our understanding of the molecular mechanisms in the progression of GBM, and these crucial as well as new diagnostic markers might be used as therapeutic targets for GBM.

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“…GAS5 inhibited osteosarcoma cell growth and metastasis by targeting miR-203a [29]. And MRPL39 hindered the progression of gastric cancer via the direct interaction with miR-130 [30]. NEAT1 was also shown to play an inhibitory action in the evolvement of several diseases.…”

Section: Discussionmentioning

confidence: 99%

Long non-coding RNA NEAT1/miR-338-3p axis impedes the progression of acute myeloid leukemia via regulating CREBRF

et al. 2020

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Background: Acute myeloid leukemia (AML) is a heterogeneous hematological disease. Our purpose of the research was to investigate the regulatory influence of long non-coding RNA (lncRNA) nuclear enriched abundant transcript 1 (NEAT1)/microRNA-338-3p (miR-338-3p)/CREB3 regulatory factor (CREBRF) in AML progression. Methods: The associated RNA and protein levels were measured by quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot, respectively. Cell growth was assessed through colony formation assay and 3-(4,5-dimethylthiazol-2-y1)-2, 5-diphenyl tetrazolium bromide (MTT) assay. Flow cytometry was exploited to determine the apoptosis rate. Cell migration and invasion were detected by transwell assay. The combination of miR-338-3p and NEAT1 or CREBRF was analyzed via the dual-luciferase reporter assay. Results: NEAT1 and CREBRF were down-regulated in AML tissues and cells. NEAT1 up-regulation suppressed cell growth, migration and invasion but enhanced apoptosis of AML cells. Inhibition of CREBRF reverted the NEAT1induced effects on AML cells. Moreover, NEAT1 directly targeted miR-338-3p and miR-338-3p targeted CREBRF. NEAT1/ miR-338-3p could affect cellular behaviors of AML cells via the modulation of CREBRF. Conclusion: NEAT1/miR-338-3p axis repressed the AML progression through regulating CREBRF, which might afford a favorable perspective for the AML treatment molecularly.

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Long Noncoding RNA MRPL39 Inhibits Gastric Cancer Proliferation and Progression by Directly Targeting miR-130

Cited by 15 publications

References 36 publications

RETRACTED: Long Noncoding RNA LOC400043 (LINC02381) Inhibits Gastric Cancer Progression Through Regulating Wnt Signaling Pathway

RETRACTED: Long Noncoding RNA LOC400043 (LINC02381) Inhibits Gastric Cancer Progression Through Regulating Wnt Signaling Pathway

Identification of Crucial Candidate Genes and Pathways in Glioblastoma Multiform by Bioinformatics Analysis

Long non-coding RNA NEAT1/miR-338-3p axis impedes the progression of acute myeloid leukemia via regulating CREBRF

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