MiR‐182 inhibits the epithelial to mesenchymal transition and metastasis of lung cancer cells by targeting the Met gene

Li, Yongwen; Zhang, Hongbing; Li, Ying; Zhao, Chenglong; Fan, Yaguang; Liu, Jinghao; Li, Xin; Liu, Hongyu; Chen, Jun

doi:10.1002/mc.22741

Cited by 60 publications

(42 citation statements)

References 24 publications

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“…For example, Yuan et al demonstrated that Notch signalling promotes the progression of non-small cell lung cancer through enhancing EMT by cross-talks with several transcriptional factors [18]. Perumal et al found PTEN inactivation induced EMT and metastasis in non-small cell lung carcinoma cells [19,20]. Zhang et al revealed that hypoxic BMSC-derived exosomal miRNAs could promote STAT3-induced EMT in lung cancer cells, and yet, promote metastasis of lung cancer [21].…”

Section: Introductionmentioning

confidence: 99%

The long noncoding RNA linc00858 promotes progress of lung cancer through miR-3182/MMP2 axis

Xue

Shi

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

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In previous studies, numerous dysregulated lncRNAs were identified using RNA-sequencing. Lung cancer is the most common malignant tumour worldwide and the second leading cause in cancer. The aim of this study is to investigate the function and mechanism of lincRNA00858 in the lung cancer. RT-PCR was used to detect the expression of lincRNA00858. Proliferation, invasion, and epithelial-mesenchymal transition (EMT) were examined by CCK8, transwell assay and western blot to evaluate the function of linc00858. Dual-luciferase reporter assay was used to identified the potential target of linc00858. Overexpression of linc00858 significantly promoted cell proliferation, invasion. We also found that linc00858 facilitated the EMT process. Dual-luciferase reporter assay revealed that linc00858 can bind with miR-3182 directly. Linc00858 can negatively regulate the expression of miR-3182. Further experiments demonstrated that MMP2 was the direct target of miR-3182. Rescue experiments revealed that linc00858 functioned through miR-3182/MMP2 axis. Taken together, we verified the role of an unknown linc00858 in lung cancer and provided its mechanism. Mechanistically, linc00858 acted as a competitive endogenous RNA to sponged miR-3182 and regulate MMP2 in lung cancer. Our study provided new clues for understanding the mechanism of lung cancer.

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Section: Introductionmentioning

confidence: 99%

The long noncoding RNA linc00858 promotes progress of lung cancer through miR-3182/MMP2 axis

Xue

Shi

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

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“…The cluster comprising miR-96, -182, and -183 was first reported in development of sensory organs ( 12 ). However, miR-182 expression has been implicated in the carcinogenesis of pancreatic carcinoma ( 13 ), glioblastoma ( 14 ), and lung cancer ( 15 ), while miR-183 expression has been reported to be involved in the carcinogenesis of osteosarcoma ( 16 ), glioblastoma ( 17 ), and pancreatic cancer ( 18 ).…”

Section: Introductionmentioning

confidence: 99%

miR-182 and miR-183 Promote Cell Proliferation and Invasion by Targeting FOXO1 in Mesothelioma

et al. 2018

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Dysregulation of miR-182 and miR-183 has been implicated in the progression of several human cancers. Our previous study showed that miR-182 and miR-183 are upregulated in malignant mesothelioma. However, their biological functions remain unclear. We performed in-situ hybridization to analyze the expression of miR-182 and miR-183 in human tissues. Functional analysis was performed by treatment of two mesothelioma cell lines (ACC-MESO1 and CRL-5915) with miR-182 and miR-183 inhibitors. RT-PCR and western blot analysis were conducted to analyze the expression of FOXO1, a known target of both miR-182 and miR-183. Mesothelioma cells treated with FOXO1 siRNA and miR-182/183 inhibitors were also analyzed by evaluating cell proliferation and invasion, as well as expression of FOXO1 and its downstream targets. We confirmed miR-182 expression in 25/29 cases and miR-183 expression in 29/29 cases of human mesothelioma tissue by in-situ hybridization. Notably, inhibition of miR-182 or miR-183 reduced cell proliferation, invasion, migration, and adhesion abilities of mesothelioma cells. Surprisingly, transfection with both miR-182 and miR-183 inhibitors showed even more effects on cell progression. Furthermore, FOXO1 was identified as a target of miR-182 and miR-183 in mesothelioma cells. Inhibition of miR-182 and miR-183 reduced cell proliferation ability via upregulation of FOXO1 and its downstream targets, namely, p27. Moreover, inhibition of miR-182 and miR-183 reduced the cell invasion properties of mesothelioma cells. Our findings indicated that miR-182 and miR-183 promote mesothelioma cell progression via downregulation of FOXO1 and p27. Targeting the miR-182/183—FOXO1 axis could serve as a novel treatment against malignant mesothelioma.

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“…EMT process and HGF/c-MET pathway are foremost molecular mechanisms of antitumor drug resistance, which significantly promotes the antitumor effect of drugs on cancer cells. [67][68][69][70][71][72][73][74][75][76][77] Jiao et al showed that HGF treatment induced gefitinib resistance in human lung cancer cells and miR-1-3 p or miR-206 sensitizes cells to gefitinib by inhibition of c-Met and EMT process. 78 In the present work, we found that ARQ-197 inhibited the EMT process of HCC cells and enhanced the sensitivity of HCC cells to sorafenib.…”

Section: Discussionmentioning

confidence: 99%

<p>ARQ-197 enhances the antitumor effect of sorafenib in hepatocellular carcinoma cells via decelerating its intracellular clearance</p>

Gao¹,

Chen²,

Huang³

et al. 2019

OTT

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Background: Hepatocellular carcinoma (HCC) is one of the heaviest malignant burdens in China. Molecular targeting agent, sorafenib, is the main therapeutic option for antitumor therapy of advanced HCC, but it is currently too expensive for the public and its therapeutic effect does not satisfy initial expectation. Therefore, it is important to develop more effective molecular targeted therapeutic strategies for advanced HCC. Materials and methods: The antitumor effects of sorafenib or ARQ-197, an antagonist of c-MET (tyrosine-protein kinase Met or hepatocyte growth factor receptor), were examined by MTT or in murine tumor model. The effect of ARQ-197 on epithelial-mesenchymal transition (EMT) or multidrug resistance (MDR) was examined by quantitative real-time PCR for the expression of related genes. The clearance of sorafenib in HCC cells was detected by liquid chromatography-mass spectrometry/mass spectrometry. Results: ARQ-197 treatment enhanced the sensitivity of HCC cells to sorafenib. Mechanistic studies indicated that ARQ-197 inhibited the expression of EMT-and MDR-related genes. Moreover, ARQ-197 treatment decelerated the clearance of sorafenib in cultured HCC cells and subcutaneous HCC tumors in nude mice. Conclusion: In the present work, our data suggested that ARQ-197 decelerated the clearance of sorafenib in HCC cells and enhanced the antitumor effect of sorafenib.

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MiR‐182 inhibits the epithelial to mesenchymal transition and metastasis of lung cancer cells by targeting the Met gene

Abstract: The microRNA miR-182, belonging to the miR-183 family, is one of the most frequently studied cancer-related oncogenic miRNAs that is dysregulated in various cancer tissues, and it plays a crucial role in tumorigenesis and tumor progression. Studies

Cited by 60 publications

References 24 publications

The long noncoding RNA linc00858 promotes progress of lung cancer through miR-3182/MMP2 axis

The long noncoding RNA linc00858 promotes progress of lung cancer through miR-3182/MMP2 axis

miR-182 and miR-183 Promote Cell Proliferation and Invasion by Targeting FOXO1 in Mesothelioma

<p>ARQ-197 enhances the antitumor effect of sorafenib in hepatocellular carcinoma cells via decelerating its intracellular clearance</p>

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