Tumor-suppressive miR-218-5p inhibits cancer cell proliferation and migration via EGFR in non-small cell lung cancer

Zhu, Kegan; Ding, Hanying; Wang, Wengong; Liao, Zhicong; Fu, Zheng; Hong, Yeting; Zhou, Yong; Zhang, Chenyu; Chen, Xi

doi:10.18632/oncotarget.8576

Cited by 73 publications

(60 citation statements)

References 45 publications

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“…To date, there are three main approaches to potential miRNA-targeting therapies: expression vectors (miRNA sponges), small-molecule inhibitors and synthetic oligonucleotides [32]. For example, aberrantly activated miRNAs can be silenced using antagomirs, and re-expression of miRNAs that are lost in cancers can be achieved by the induction of miRNA mimics [18, 33, 34]. It has been found that aberrant expression of the miR-520 family occurs in malignant tumours, and transcripts in this miRNA family have been identified as key regulators of oncogenes [35].…”

Section: Discussionmentioning

confidence: 99%

A Novel Role for MiR-520a-3p in Regulating EGFR Expression in Colorectal Cancer

Zhang

Liu

et al. 2017

Cell Physiol Biochem

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Background/Aims: MicroRNAs (miRNAs) have been consistently demonstrated to be involved in colorectal cancer as either tumour oncogenes or tumour suppressors. However, the detailed role of miR-520a-3p in colorectal cancer remains poorly understood. Methods: Quantitative RT-PCR and western blotting assays were used to measure miR-520a-3p and EGFR expression levels in colorectal cancer tissues, respectively. Luciferase reporter assay was employed to validate the direct targeting of EGFR by miR-520a-3p. Cell migration, apoptosis and cell cycle assays were performed to analyse the biological functions of miR-520a-3p and EGFR in colorectal cancer cells. In vivo experiment was performed to analyse the effects of miR-520a-3p and EGFR on the growth of colorectal cancer xenografts in mice. Results: In this study, we found that miR-520a-3p was most likely to target the EGFR 3’-UTR, which was experimentally validated. In addition, we investigated the biological effects of EGFR inhibition by miR-520a-3p both in vitro and In vivo and found that miR-520a-3p could suppress cell migration, promote apoptosis, lead to colorectal cancer cell cycle arrest at the G0/G1 phase, and decelerate tumour growth in xenograft mice, potentially by targeting EGFR. Conclusions: This study highlights a tumour suppressor role for miR-520a-3p in colorectal cancer via the regulation of EGFR expression. Thus, miR-520a-3p may be a novel molecular therapeutic target for colorectal cancer.

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Section: Discussionmentioning

confidence: 99%

A Novel Role for MiR-520a-3p in Regulating EGFR Expression in Colorectal Cancer

Zhang

Liu

et al. 2017

Cell Physiol Biochem

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“…Mir-199b shows upregulation in p53R172H iPS. The same is true for miR-218, an miRNA that seems to acts as a tumour suppressor 72, 73 and promotes stem cell differentiation. 74, 75, 76 The tumour suppressive miR-708 and miR-126 on the other hand are upregulated during reprogramming in p53 wt cells and reduced in p53R172H cells.…”

Section: Resultsmentioning

confidence: 83%

Differential regulated microRNA by wild type and mutant p53 in induced pluripotent stem cells

et al. 2016

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The tumour suppressor p53 plays an important role in somatic cell reprogramming. While wild-type p53 reduces reprogramming efficiency, mutant p53 exerts a gain of function activity that leads to increased reprogramming efficiency. Furthermore, induced pluripotent stem cells expressing mutant p53 lose their pluripotency in vivo and form malignant tumours when injected in mice. It is therefore of great interest to identify targets of p53 (wild type and mutant) that are responsible for this phenotype during reprogramming, as these could be exploited for therapeutic use, that is, formation of induced pluripotent stem cells with high reprogramming efficiency, but no oncogenic potential. Here we studied the transcriptional changes of microRNA in a series of mouse embryonic fibroblasts that have undergone transition to induced pluripotent stem cells with wild type, knock out or mutant p53 status in order to identify microRNAs whose expression during reprogramming is dependent on p53. We identified a number of microRNAs, with known functions in differentiation and carcinogenesis, the expression of which was dependent on the p53 status of the cells. Furthermore, we detected several uncharacterised microRNAs that were regulated differentially in the different p53 backgrounds, suggesting a novel role of these microRNAs in reprogramming and pluripotency.

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“…The correlation between EGFR protein levels and miR‐218‐5p is an inverse correlation in NSCLC. The expression of EGFR is negatively regulated by mir‐218 , which leads to inhibiting EGFR translation in NSCLC (Figure ) …”

Section: Tumor Suppressor Micrornasmentioning

confidence: 99%

Tumor suppressor microRNAs in lung cancer: An insight to signaling pathways and drug resistance

Asghariazar

Sakhinia

Mansoori

et al. 2019

J of Cellular Biochemistry

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Lung cancer (LC) is the second common cancer for both women and men all over the world. Unfortunately, the number of LC deaths is increasing rapidly each year so early diagnosis of LC can be lifesaving. MicroRNAs are involved in multiple processes, such as cell differentiation, transcription, inflammation, proliferation, cell signaling, and apoptosis. In LC, microRNAs function as tumor suppressors (TS) or oncogenes depending on the targets. Changes in microRNAs expression level are related to tumor initiation, progression, and metastasis. MicroRNAs can regulate gene expression and thus affect the activity status of different signaling pathways including AKT, JAK-STAT, MAPK, TGF-β, WNT, and ERK signaling pathways. Positive or negative effects on drug resistance of LC are directly affected by microRNAs and their target genes. MicroRNAs can be beneficial in combination therapy with other drugs and chemotherapeutic agents for LC. K E Y W O R D S drug resistance, lung cancer, microRNA, signaling pathways, tumor suppressor How to cite this article: Asghariazar V, Sakhinia E, Mansoori B, Mohammadi A, Baradaran B. Tumor suppressor microRNAs in lung cancer: An insight to signaling pathways and drug resistance.

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Tumor-suppressive miR-218-5p inhibits cancer cell proliferation and migration via EGFR in non-small cell lung cancer

Cited by 73 publications

References 45 publications

A Novel Role for MiR-520a-3p in Regulating EGFR Expression in Colorectal Cancer

A Novel Role for MiR-520a-3p in Regulating EGFR Expression in Colorectal Cancer

Differential regulated microRNA by wild type and mutant p53 in induced pluripotent stem cells

Tumor suppressor microRNAs in lung cancer: An insight to signaling pathways and drug resistance

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