Low miR-145 silenced by DNA methylation promotes NSCLC cell proliferation, migration and invasion by targeting mucin 1

Ye, Zhiqiang; Shen, Ning; Weng, Yimin; Li, Kai; Liu, Hu; Liao, Hongyin; An, Jun; Liu, Libao; Lao, Sen; Cai, Sanjun

doi:10.1080/15384047.2015.1046024

Cited by 25 publications

(19 citation statements)

References 36 publications

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“…Lu et al (18) showed that miR-145 inhibited the migration and invasion of glioma cells via direct inhibition of ADAM17 expression. Zhang et al (19) reported that miR-145 suppressed the invasion and metastasis Only few studies have focused on the underlying molecular mechanism of the involvement of miR-145 in the development and progression of NSCLC (20). The present study identified one of its targets, FSCN1, which is involved in the miR-145-mediated downregulation of NSCLC cell migration and invasion.…”

Section: A B Discussionmentioning

confidence: 59%

MicroRNA-145 inhibits migration and invasion via inhibition of fascin 1 protein expression in non-small-cell lung cancer cells

Zhang

Zhou

et al. 2015

Molecular Medicine Reports

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MicroRNA (miR)-145 has been shown to act as a suppressor in numerous cancer types, including non-small-cell lung cancer (NSCLC). Fascin 1 (FSCN1), an actin bundling protein, has been implicated in NSCLC. However, the detailed role of miR-145 as well as the association between miR-145 and FSCN1 in the regulation of migration and invasion in NSCLC cells has remained elusive. The present study revealed that miR-145 was downregulated and FSCN1 was upregulated in NSCLC tissues and cell lines. Further investigation showed that overexpression of miR-145 markedly inhibited the protein expression of FSCN1, while knockdown of miR-145 upregulated the protein (but not mRNA) levels of FSCN1 in the NSCLC cell line H129. Moreover, a luciferase reporter assay indicated that FSCN1 is a direct target of miR-145 in NSCLC H129 cells. Furthermore, overexpression of miR-145 markedly inhibited the migration and invasion of NSCLC cells, similar to the effect of small interfering RNA-mediated FSCN1 inhibition in H129 cells. In addition, the inhibitory effect of miR-145 overexpression on migration and invasion was reversed by FSCN1 upregulation in H129 cells. These findings suggested that miR-145 has an inhibitory effect on the migration and invasion in NSCLC cells, at least in part through suppressing the protein expression of its target FSCN1. Therefore, miR-145/FSCN1 may be used as a potential target for the treatment of NSCLC.

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Section: A B Discussionmentioning

confidence: 59%

MicroRNA-145 inhibits migration and invasion via inhibition of fascin 1 protein expression in non-small-cell lung cancer cells

Zhang

Zhou

et al. 2015

Molecular Medicine Reports

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“…miR-145 inhibits migration and invasion by downregulating FSCN1 (17) and mucin1 (18). A previous study by the present authors revealed that miR-145 acts as a metastasis suppressor by targeting metadherin in lung cancer (33).…”

Section: Discussionmentioning

confidence: 99%

“…miR-145 regulates chemoresistance in hepatocellular carcinoma (15) and bladder cancer (16) via EMT. miR-145 inhibits migration and invasion by down-regulating fascin actin-bundling protein 1 (FSCN1) (17) and mucin 1 (18).…”

Section: Introductionmentioning

confidence: 99%

miR‑145‑5p inhibits epithelial‑mesenchymal transition via the JNK signaling pathway by targeting MAP3K1 in non‑small cell lung cancer cells

et al. 2017

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Abstract. Lung cancer is one of the most common types of tumors and the leading cause of cancer-associated mortality in the world. Additionally, non-small cell lung cancer (NSCLC) accounts for ~80% of all lung cancer cases. Epithelialmesenchymal transition (EMT) is an important cell biological process, which is associated with cancer migration, metastasis, asthma and fibrosis in the lung. In the present study, it was revealed that miR-145-5p was able to suppress EMT by inactivating the c-Jun N-terminal kinase (JNK) signaling pathway in NSCLC cells. Mitogen-activated protein kinase kinase kinase 1 (MAP3K1) was predicted and confirmed to be a novel target of miR-145-5p. Overexpression of MAP3K1 was able to reverse the inhibition of EMT induced by miR-145-5p via the JNK signaling pathway. Overall, the results revealed that miR-145-5p inhibits EMT via the JNK signaling pathway by targeting MAP3K1 in NSCLC cells.

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“…36 In NSCLC, miR-145-5p has been reported to be downregulated and to exert tumor-suppressor functions. Some targets of miR-145-5p in NSCLC have been reported, such as c-Myc, 37 mucin 1, 38 and FSCN1. 39 Despite these discoveries, the precise molecular mechanisms of miRNA-145-5p in NSCLC remain largely unknown and require further exploration.…”

Section: Introductionmentioning

confidence: 99%

Clinical value of miR-145-5p in NSCLC and potential molecular mechanism exploration: A retrospective study based on GEO, qRT-PCR, and TCGA data

et al. 2017

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MicroRNAs have been reported to be involved in various biological processes. Here, we performed a systematic analysis to explore the clinical value and potential molecular mechanism of miR-145-5p in non-small cell lung cancer. First, a meta-analysis was performed with eligible literature, followed by microRNA microarrays in the Gene Expression Omnibus database, to verify the diagnostic and prognostic values of miR-145-5p. A cohort of 125 clinical paired non-small cell lung cancer samples was next used to detect the level of miR-145-5p and to explore the relationship of miR-145-5p with clinicopathological parameters. The Cancer Genome Atlas database was additionally applied to investigate the role of miR-145-5p in non-small cell lung cancer. The potential targets of miR-145-5p were predicted using 12 online prediction databases to explore the prospective molecular mechanism of miR-145-5p in non-small cell lung cancer. The expression of miR-145-5p in non-small cell lung cancer was significantly lower than that in healthy tissues. And miR-145-5p tended to show better diagnostic performance in lung squamous cell carcinoma than in lung adenocarcinoma. Furthermore, the expression of miR-145-5p was closely associated with lymph node metastasis in non-small cell lung cancer. Gene ontology enrichment and Kyoto Encyclopedia of Genes and Genomes pathway analysis revealed that the target genes were mainly enriched with enzyme-linked receptor protein signaling pathways, SH3 domain binding, cell leading edge, and adherens junction. The protein-protein interaction network showed that eight hub genes (SMAD4, SMAD2, IRS1, FOXO1, ERBB4, NRAS, ACTB, and ACTG1) might be the key target genes of miR-145-5p in non-small cell lung cancer. The information we obtained might offer new perspectives for clinical diagnosis and treatment for non-small cell lung cancer.

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Low miR-145 silenced by DNA methylation promotes NSCLC cell proliferation, migration and invasion by targeting mucin 1

Cited by 25 publications

References 36 publications

MicroRNA-145 inhibits migration and invasion via inhibition of fascin 1 protein expression in non-small-cell lung cancer cells

MicroRNA-145 inhibits migration and invasion via inhibition of fascin 1 protein expression in non-small-cell lung cancer cells

miR‑145‑5p inhibits epithelial‑mesenchymal transition via the JNK signaling pathway by targeting MAP3K1 in non‑small cell lung cancer cells

Clinical value of miR-145-5p in NSCLC and potential molecular mechanism exploration: A retrospective study based on GEO, qRT-PCR, and TCGA data

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