microRNA-361 targets Wilms' tumor 1 to inhibit the growth, migration and invasion of non-small-cell lung cancer cells

Yang, S X; Zhang, Yingchao; Zhao, Xin; Wang, Jingzheng; Shang, Jianjing

doi:10.3892/mmr.2016.5858

Cited by 16 publications

(17 citation statements)

References 43 publications

(47 reference statements)

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“…Mir466i was upregulated in NLPs, while Mir7007, mmu-mir-703, Mir107, Mir361, Mir6918, Mir6982 , and Mir3099 were downregulated in NLPs. Among these miRNAs, Mir107 (Chen et al, 2013; Song et al, 2015; Xia et al, 2016; Yang et al, 2016) and Mir361 (Wu et al, 2013; Jacques et al, 2014; Chen et al, 2016; Sun et al, 2016) have been reported to suppress tumor growth and stem cell growth. However, none of the eight miRNAs have been reported previously in the inner ear and need to be further studied in the future.…”

Section: Discussionmentioning

confidence: 99%

Characterization of Lgr5+ Progenitor Cell Transcriptomes after Neomycin Injury in the Neonatal Mouse Cochlea

Zhang

Yu³

et al. 2017

Front. Mol. Neurosci.

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Lgr5+ supporting cells (SCs) are enriched hair cell (HC) progenitors in the cochlea. Both in vitro and in vivo studies have shown that HC injury can spontaneously activate Lgr5+ progenitors to regenerate HCs in the neonatal mouse cochlea. Promoting HC regeneration requires the understanding of the mechanism of HC regeneration, and this requires knowledge of the key genes involved in HC injury-induced self-repair responses that promote the proliferation and differentiation of Lgr5+ progenitors. Here, as expected, we found that neomycin-treated Lgr5+ progenitors (NLPs) had significantly greater HC regeneration ability, and greater but not significant proliferation ability compared to untreated Lgr5+ progenitors (ULPs) in response to neomycin exposure. Next, we used RNA-seq analysis to determine the differences in the gene-expression profiles between the transcriptomes of NLPs and ULPs from the neonatal mouse cochlea. We first analyzed the genes that were enriched and differentially expressed in NLPs and ULPs and then analyzed the cell cycle genes, the transcription factors, and the signaling pathway genes that might regulate the proliferation and differentiation of Lgr5+ progenitors. We found 9 cell cycle genes, 88 transcription factors, 8 microRNAs, and 16 cell-signaling pathway genes that were significantly upregulated or downregulated after neomycin injury in NLPs. Lastly, we constructed a protein-protein interaction network to show the interaction and connections of genes that are differentially expressed in NLPs and ULPs. This study has identified the genes that might regulate the proliferation and HC regeneration of Lgr5+ progenitors after neomycin injury, and investigations into the roles and mechanisms of these genes in the cochlea should be performed in the future to identify potential therapeutic targets for HC regeneration.

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Section: Discussionmentioning

confidence: 99%

Characterization of Lgr5+ Progenitor Cell Transcriptomes after Neomycin Injury in the Neonatal Mouse Cochlea

Zhang

Yu³

et al. 2017

Front. Mol. Neurosci.

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“…Although advances have been made on lung cancer intervention, the outcomes of patients remain very poor. The five-year survival rate of patients with NSCLC remains low (5). Therefore, to improve the outcome of NSCLC the identification of novel biomarkers for NSCLC diagnosis and prognosis and the development of effective therapeutic targets are urgently required.…”

Section: Introductionmentioning

confidence: 99%

“…An increasing number of studies indicate that miRs are critical for the regulation of nearly all physiological processes, including the cell cycle, proliferation, migration, invasion and differentiation of cells (8). Therefore, abnormal expression of miRs typically results in occurrence of human cancer, including NSCLC (5). For example, upregulation of miR-383 has been demonstrated to inhibit the proliferation, migration and invasion of colon cancer cells (9).…”

Section: Introductionmentioning

confidence: 99%

Overexpression of microRNA‑936 suppresses non‑small cell lung cancer cell proliferation and invasion via targeting E2F2

Zhou

Tao

2018

Exp Ther Med

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MicroRNA (miR)-936 has been reported to inhibit the cell cycle and glioma cell proliferation. However, the roles of miR-936 in other human tumors remain largely unknown. In the present study, it was indicated that miR-936 was significantly downregulated in non-small cell lung cancer (NSCLC) tissues compared with adjacent normal tissues by reverse transcription-quantitative polymerase chain reaction (RT-qPCR). Results also indicated that miR-936 was downregulated in NSCLC cell lines compared with 16HBE cells. Furthermore, it was demonstrated that overexpression of miR-936 significantly inhibited the proliferation, cell cycle progression and invasion of NSCLC cells. Notably, E2F2 was identified as a target gene of miR-936 in NSCLC cells. The results indicated that E2F2 was upregulated in NSCLC tissues and cell lines, and its expression was negatively correlated with that of miR-936 in NSCLC tissues. Overexpression of miR-936 significantly reduced the protein expression levels of E2F2 in NSCLC cells. Furthermore, restoration of E2F2 rescued the proliferation and invasion of NSCLC cells transfected with miR-936 mimics. To the best of our knowledge, the present findings demonstrated for the first time that miR-936 suppressed NSCLC progression by directly targeting E2F2.

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“…Previous efforts to characterize patients with LC who will develop BM have been disappointing [13]; thus, we resort to molecular mechanisms in order to provide a more accurate evaluation of patients with BM from LC. MicroRNAs (miRNAs) are non-coding RNAs of approximately [18][19][20][21][22][23][24] nucleotides that can bind to the sequences of target mRNAs in the 3'-untranslated region (3'-UTR) and modulate gene expression at the post-transcriptional level [16,17], therefore affecting a wide variety of biological processes, including proliferation, differentiation as well as and apoptosis. Thus, these miRNAs are associated with a diverse array of human diseases, including cancer [18][19][20].…”

Section: Introductionmentioning

confidence: 99%

“…MicroRNAs (miRNAs) are non-coding RNAs of approximately [18][19][20][21][22][23][24] nucleotides that can bind to the sequences of target mRNAs in the 3'-untranslated region (3'-UTR) and modulate gene expression at the post-transcriptional level [16,17], therefore affecting a wide variety of biological processes, including proliferation, differentiation as well as and apoptosis. Thus, these miRNAs are associated with a diverse array of human diseases, including cancer [18][19][20]. The altered expression of miRNAs has been commonly found in LC [21,22], and accumulatively been evidenced to involve in carcinogenesis and tumor progression in LC [23][24][25].…”

Section: Introductionmentioning

confidence: 99%

Downregulation of MicroRNA-330 Correlates with the Radiation Sensitivity and Prognosis of Patients with Brain Metastasis from Lung Cancer

Jiang

Zhu²,

Zhang

et al. 2017

Cell Physiol Biochem

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Background: The present study sought to explore the role of in predicting the radiation response and prognosis of patients with brain metastasis (BM) from lung cancer (LC). Methods: Patients with BM from LC were identified and classified into radiation-sensitive and radiation-resistant groups according to the overall survival rate, local and distant recurrence rate after conventional whole-brain radiation therapy. Quantitative realtime polymerase chain reaction (qRT-PCR) was used to detect miR-330 expression in serum. Receiver operating characteristic (ROC) curves were used to evaluate the prognostic value of miR-330 for the radiation sensitivity of brain metastasis from LC. Related clinical factors for radiation sensitivity were assessed by logistic regression analysis, and a survival analysis was conducted using COX regression and the Kaplan-Meier method. Results: MiR-330 exhibited lower expression in the radiation-sensitive group than in the radiation-resistant group. The area under the ROC curve of miR-330 for predicting radiation sensitivity was 0.898 (optimal cut-off value, 0.815), with a sensitivity of 71.7% and a specificity of 90.1%. After radiation therapy, patients with low miR-330 expression, compared to patients with high miR-330 expression, displayed a lower survival rate and a median survival time. MiR-330 expression was correlated with extracranial metastasis, maximum BM diameter, tumor-node-metastasis (TNM) stage and node (N) stage. Logistic regression and COX regression analyses revealed that extracranial metastasis, TNM stage, N stage and miR-330 expression were factors that influenced both radiation sensitivity and individual prognostic factors in patients with BM from LC. Conclusions: These findings indicate that the downregulation of miR-330 correlates with radiation sensitivity and poor prognosis in patients with BM from LC.

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microRNA-361 targets Wilms' tumor 1 to inhibit the growth, migration and invasion of non-small-cell lung cancer cells

Cited by 16 publications

References 43 publications

Characterization of Lgr5+ Progenitor Cell Transcriptomes after Neomycin Injury in the Neonatal Mouse Cochlea

Characterization of Lgr5+ Progenitor Cell Transcriptomes after Neomycin Injury in the Neonatal Mouse Cochlea

Overexpression of microRNA‑936 suppresses non‑small cell lung cancer cell proliferation and invasion via targeting E2F2

Downregulation of MicroRNA-330 Correlates with the Radiation Sensitivity and Prognosis of Patients with Brain Metastasis from Lung Cancer

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