MicroRNAs and Metastasis

Solé, Carla; Lawrie, Charles H.

doi:10.3390/cancers12010096

Cited by 18 publications

(13 citation statements)

References 184 publications

(181 reference statements)

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“…MicroRNAs (miRs/miRNAs) are non-coding, single- stranded RNA molecules of ~22 nucleotides in length, encoded by endogenous genes ( 22 ). The abnormal expression of miRNAs has been reported in various types of cancer, such as hepatocellular carcinoma, gastric cancer and retinoblastoma ( 23 , 24 ). Notably, previous studies have demonstrated that miR-1236-3p inhibited the migration and invasion of A549 and ovarian cancer cells by targeting Kruppel-like factor 8 or zinc finger E-box-binding homeobox 1 ( 25 , 26 ).…”

Section: Introductionmentioning

confidence: 99%

lncRNA FEZF1‑AS1 promotes migration, invasion and epithelial‑mesenchymal transition of retinoblastoma cells by targeting miR‑1236‑3p

Zhang

Yang²,

et al. 2020

Mol Med Rep

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long non-coding rnas (lncrnas) and micrornas (mirs) have been reported to regulate disease progression in numerous types of disease, including retinoblastoma (rb). Therefore, the present study aimed to investigate the effects of the lncRNA FEZ family zinc finger 1 antisense RNA 1 (FEZF1-AS1) on Rb and to determine its possible mechanism of action. reverse transcription-quantitative Pcr and western blot analysis were conducted to detect the gene or protein expression. cell counting Kit-8, wound healing and transwell invasion assays were performed to estimate the capabilities of cell viability, invasion and migration. The potential association between FEZF1-AS1 and miR-1236-3p in Y79 cells was measured via dual-luciferase reporter assay. The results of the present study revealed that the levels of FEZF1-AS1 were significantly upregulated in different Rb cell lines, with the most prominent upregulation observed in Y79 cells. In addition, the cell viability, invasive and migratory abilities, and the ability to undergo epithelial-mesenchymal transition (eMT), were significantly inhibited following the transfection of short hairpin RNA (shRNA)-FEZF1-AS1 into Y79 cells. Further experimental validation confirmed that miR-1236-3p may be a direct target of FEZF1-AS1. Notably, the miR-1236-3p inhibitor was discovered to reverse the inhibitory effects of shRNA-FEZF1-AS1 on cell viability, invasion, migration and EMT. In conclusion, the findings of the present study suggested that lncRNA-FEZF1-AS1 may promote the viability, migration, invasion and EMT of Rb cells by modulating miR-1236-3p.

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Section: Introductionmentioning

confidence: 99%

lncRNA FEZF1‑AS1 promotes migration, invasion and epithelial‑mesenchymal transition of retinoblastoma cells by targeting miR‑1236‑3p

Zhang

Yang²,

et al. 2020

Mol Med Rep

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“…MicroRNAs (miRNAs) are a class of single-stranded noncoding RNA that can directly bind to the 3'-untranslated region of their target mRNAs, which triggers mRNA degradation and/or translation depression (14). Studies have shown that aberrant miRNA expression is closely associated with the initiation and development of NSCLC, and is implicated in the regulation of a wide range of tumorigenic behaviors (15)(16)(17).…”

Section: Introductionmentioning

confidence: 99%

Long noncoding RNA CBR3 antisense RNA 1 promotes the aggressive phenotypes of non‑small‑cell lung cancer by sponging microRNA‑509‑3p and competitively upregulating HDAC9 expression

et al. 2020

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Long noncoding RNA CBR3 antisense RNA 1 (CBR3-AS1) plays significant roles in the initiation and progression of osteosarcoma. The aim of the present study was to investigate the involvement of CBR3-AS1 in the development of non-small cell lung cancer (NSCLC). Reverse transcription-quantitative PCR was performed to detect CBR3-AS1 expression in NSCLC tissues and cell lines. The impacts of CBR3-AS1 on cellular proliferation, apoptosis, migration and invasiveness in vitro , and tumor growth in vivo , were investigated using the Cell Counting Kit-8 assay, flow cytometry, Transwell migration and invasion assays, and tumor xenograft model-based analysis, respectively. The results indicated that CBR3-AS1 was markedly upregulated in NSCLC tissues and cell lines. High CBR3-AS1 expression was correlated with larger tumor size, advanced TNM stage, increased incidence of lymph node metastasis and shorter overall survival times in patients with NSCLC. Furthermore, CBR3-AS1-knockdown notably suppressed cellular proliferation, migration and invasiveness in vitro , and also promoted apoptosis and suppressed tumorigenicity in vivo . Mechanistic investigation demonstrated that CBR3-AS1 functions as a competing endogenous RNA for microRNA-509-3p (miR-509-3p) in NSCLC cells. Furthermore, miR-509-3p exerted tumor-suppressive effects in NSCLC, and histone deacetylase 9 (HDAC9) was identified as a direct target of miR-509-3p. HDAC9 expression was suppressed by CBR3-AS1 depletion, which was abolished by miR-509-3p inhibition. Further rescue experiments revealed that increasing the output of the miR-509-3p/HDAC9 axis counteracted the CBR3-AS1 depletion-induced inhibitory effects on NSCLC cells. Collectively, the results of the present study indicate that the CBR3-AS1/miR-509-3p/HDAC9 pathway exerts tumor-promoting actions in NSCLC oncogenesis and progression, suggesting that this pathway is an effective target for the management of NSCLC.

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“…Regarding EOC, a substantial amount of evidence has established that various lncRNAs are differentially expressed and function as tumor-inhibiting or tumor-promoting factors in regulating tumorigenesis [15][16][17]. microRNAs (miRNAs) are a class of single-stranded, non-coding RNA transcripts comprising [17][18][19][20][21][22][23][24] nucleotides [18]. These short miRNAs bind to the 3′-untranslated region (3′-UTRs) of their target genes through miRNA-response elements by complete or incomplete complementary base pairing, which results in translation suppression or target mRNA degradation [19].…”

Section: Introductionmentioning

confidence: 99%

Long non-coding RNA PTPRG-AS1 promotes cell tumorigenicity in epithelial ovarian cancer by decoying microRNA-545-3p and consequently enhancing HDAC4 expression

Shi

Zhang

et al. 2020

Preprint

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Background: Long non-coding RNA PTPRG antisense RNA 1 (PTPRG-AS1) deregulation has been reported in various human malignancies and identified as an important modulator of cancer development. Few reports have focused on the detailed role of PTPRG-AS1 in epithelial ovarian cancer (EOC) and its underlying mechanism. This study aimed to determine the physiological function of PTPRG-AS1 in EOC. A series of experiments were also performed to identify the mechanisms through which PTPRG-AS1 exerts its function in EOC.Methods: Reverse transcription-quantitative polymerase chain reaction was used to determine PTPRG-AS1 expression in EOC tissues and cell lines. PTPRG-AS1 was silenced in EOC cells and studied with respect to cell proliferation, apoptosis, migration, and invasion in vitro and tumor growth in vivo. The putative miRNAs that target PTPRG-AS1 were predicted using bioinformatics analysis and further confirmed in luciferase reporter and RNA immunoprecipitation assays.Results: Our data verified the upregulation of PTPRG-AS1 in EOC tissues and cell lines. High PTPRG-AS1 expression was associated with shorter overall survival in patients with EOC. Functionally, EOC cell proliferation, migration, invasion in vitro, and tumor growth in vivo were suppressed by PTPRG-AS1 silencing. In contrast, cell apoptosis was promoted by loss of PTPRG-AS1. Regarding the mechanism, PTPRG-AS1 could serve as a competing endogenous RNA in EOC cells by decoying microRNA-545-3p (miR-545-3p), thereby elevating histone deacetylase 4 (HDAC4) expression. Furthermore, rescue experiments revealed that PTPRG-AS1 knockdown-mediated effects on EOC cells were, in part, counteracted by the inhibition of miR-545-3p or restoration of HDAC4.Conclusions: PTPRG-AS1 functioned as an oncogenic lncRNA that aggravated the malignancy of EOC through the miR-545-3p/HDAC4 ceRNA network. Thus, targeting the PTPRG-AS1/miR-545-3p/HDAC4 pathway may be a novel strategy for EOC anticancer therapy.

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MicroRNAs and Metastasis

Cited by 18 publications

References 184 publications

lncRNA FEZF1‑AS1 promotes migration, invasion and epithelial‑mesenchymal transition of retinoblastoma cells by targeting miR‑1236‑3p

lncRNA FEZF1‑AS1 promotes migration, invasion and epithelial‑mesenchymal transition of retinoblastoma cells by targeting miR‑1236‑3p

Long noncoding RNA CBR3 antisense RNA 1 promotes the aggressive phenotypes of non‑small‑cell lung cancer by sponging microRNA‑509‑3p and competitively upregulating HDAC9 expression

Long non-coding RNA PTPRG-AS1 promotes cell tumorigenicity in epithelial ovarian cancer by decoying microRNA-545-3p and consequently enhancing HDAC4 expression

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