MicroRNA-374b inhibits the tumor growth and promotes apoptosis in non-small cell lung cancer tissue through the p38/ERK signaling pathway by targeting JAM-2

Wang, Yujun; Yu, Lijuan; Wang, Tao

doi:10.21037/jtd.2018.09.93

Cited by 14 publications

(10 citation statements)

References 21 publications

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“…Increasing evidence has demonstrated that numerous miRNAs are dysregulated in NScLc and that this dysregulation is a hallmark of NScLc (30)(31)(32). Recently, miRNAs have been identified as a novel player in gene regulation in NSCLC, with aberrant miRNAs expression serving pivotal roles in formation and progression of NScLc (33)(34)(35). A detailed investigation of cancer-associated miRNAs in NScLc is therefore crucial for identifying effective therapeutic targets for this disease.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-625 inhibits the progression of non‑small cell lung cancer by directly targeting HOXB5 and deactivating the Wnt/β-catenin pathway

Tan

Jiang

et al. 2019

Int J Mol Med

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Numerous microRNAs (miRs) are dysregulated in non-small cell lung cancer (NScLc), serving pivotal roles in its formation and progression. miR-625 is dysregulated in several types of human cancer, but its involvement in the formation and development of NScLc remains poorly understood. In the present study, we aimed to investigate miR-625 expression in NScLc and its role in regulating NScLc cell behavior. miR-625 expression in NScLc tissues and cell lines was detected using reverse transcription-quantitative polymerase chain reaction. The effects of miR-625 overexpression on NScLc cell proliferation, apoptosis, migration and invasion in vitro were assessed using an MTT assay, flow cytometry, and cell migration and invasion assays, respectively. The effects of miR-625 upregulation on NScLc growth were evaluated in an in vivo xenograft model. The molecular mechanisms underlying the tumor-suppressing roles of miR-625 in NScLc were explored in detail. miR-625 expression was determined to be downregulated in NScLc tissues and cell lines. This decreased expression was associated with advanced clinical features and poor overall survival of patients with NScLc. Exogenous miR-625 expression suppressed NScLc cell proliferation, migration and invasion, and induced apoptosis in vitro. miR-625 upregulation hindered NScLc tumor growth in vivo. Homeobox B5 (HOXB5) was proposed to be the direct target gene of miR-625 in NScLc cells. The tumor-suppressing effects of HOXB5 silencing were similar to those of miR-625 overexpression in NScLc cells. In rescue experiments, HOXB5 overexpression partially reversed the inhibitory effects of miR-625 in NScLc cells. miR-625 upregulation directly targeted HOXB5 to deactivate the Wnt/β-catenin signaling pathway in NScLc cells in vitro and in vivo. miR-625 was determined to be associated with HOXB5 suppression and Wnt/β-catenin pathway deactivation, which in turn inhibited the aggressive behavior of NScLc cells in vitro and in vivo.

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Section: Discussionmentioning

confidence: 99%

MicroRNA-625 inhibits the progression of non‑small cell lung cancer by directly targeting HOXB5 and deactivating the Wnt/β-catenin pathway

Tan

Jiang

et al. 2019

Int J Mol Med

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“…Tumorigenesis is a multistep process involving genetic and epigenetic alterations [ 7 ]. Epigenetics is a fundamental regulatory mechanism of gene expression that involves DNA methylation, histone modification, noncoding RNA regulation, and chromatin remodeling [ 8 – 11 ]. Epigenetic abnormalities are reportedly involved in tumor initiation, progression, and recurrence [ 12 , 13 ].…”

Section: Introductionmentioning

confidence: 99%

Development and validation of a nomogram with an epigenetic signature for predicting survival in patients with lung adenocarcinoma

Wang

Tang

et al. 2020

aging

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“…miRNAs have broad effects on a wide range of biological behaviors, including cell proliferation, cell cycle, apoptosis, differentiation, metabolism, epithelial-mesenchymal transition, and metastasis 11,12,13. In particular, numerous miRNAs were identified to be dysregulated in NSCLC, including miR-374b,14 miR-500,15 miR-628,15 and miR-647 16. miRNAs may exert tumor-suppressive or oncogenic roles in the formation and progression of NSCLC based on the biological function of their target genes 17.…”

Section: Introductionmentioning

confidence: 99%

<p>microRNA-612 suppresses the malignant development of non-small-cell lung cancer by directly targeting bromodomain-containing protein 4</p>

Kang

Kong

et al. 2019

OTT

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Background: Aberrant expression of microRNAs (miRNAs) in non-small-cell lung cancer (NSCLC) has been reported. Dysregulation of miRNAs exerts tumor-suppressing or tumor-promoting actions on the pathology and biological behaviors of NSCLC. miR-612 is associated with many types of human cancer; however, the expression, potential roles, and regulatory mechanisms of miR-612 in NSCLC remain unclear. Material and methods: Here, the expression level of miR-612 in NSCLC tissue specimens and a panel of cell lines were evaluated by RT-qPCR. Cell-Counting Kit 8, flow cytometry, Transwell migration and invasion, and in vivo tumor growth assays were performed to determine the functional role of miR-612 in malignant phenotypes of NSCLC cells. The molecular mechanism underlying the tumor-suppressive roles of miR-612 in NSCLC was investigated. Results: miR-612 was expressed at low levels in NSCLC, and low miR-612 expression was significantly correlated with TNM stage and lymph node metastasis. NSCLC patients with low miR-612 expression had shorter overall survival rate than those with high levels. Exogenous miR-612 expression decreased proliferation, migration, and invasion, and promoted apoptosis of NSCLC cells in vitro . miR-612 upregulation hindered NSCLC tumor growth in vivo . Bromodomain-containing protein 4 ( BRD4 ) was confirmed as a direct target gene of miR-612 in NSCLC cells. BRD4 was obviously overexpressed in human NSCLC tissues and inverse correlated with miR-612 expression. Inhibition of BRD4 expression simulated the tumor-suppressive functions of miR-612 overexpression in NSCLC cells. Reintroduction of miR-612 expression abrogated the miR-612-mediated suppressive effects on NSCLC cells. BRD4 upregulation inhibited activation of the PI3K/Akt pathway in NSCLC cells in vitro and in vivo . Conclusion: This study supports the first evidence that miR-612 exerts tumor-suppressive roles in the aggressive behaviors of NSCLC cells in vitro and in vivo through direct targeting BRD4 and deactivating the PI3K/Akt pathway. Thus, miR-612 might be a promising target for anticancer therapies in patients with NSCLC.

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MicroRNA-374b inhibits the tumor growth and promotes apoptosis in non-small cell lung cancer tissue through the p38/ERK signaling pathway by targeting JAM-2

Cited by 14 publications

References 21 publications

MicroRNA-625 inhibits the progression of non‑small cell lung cancer by directly targeting HOXB5 and deactivating the Wnt/β-catenin pathway

MicroRNA-625 inhibits the progression of non‑small cell lung cancer by directly targeting HOXB5 and deactivating the Wnt/β-catenin pathway

Development and validation of a nomogram with an epigenetic signature for predicting survival in patients with lung adenocarcinoma

<p>microRNA-612 suppresses the malignant development of non-small-cell lung cancer by directly targeting bromodomain-containing protein 4</p>

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