MicroRNA-409-3p Functions as a Tumor Suppressor in Human Lung Adenocarcinoma by Targeting c-Met

Wan, Li; Zhu, Lingjun; Xu, Jianghao; Lu, Binfeng; Yang, Yucai; Liu, Fengzhen; Wang, Zhaoxia

doi:10.1159/000366337

Cited by 50 publications

(49 citation statements)

References 31 publications

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“…MET is also called hepatocyte growth factor receptor (HGFR) [7]. MET is an oncogene protein with tyrosine kinase activity and is so far the uniquely detected receptor for mitogenic factor HGF [8].…”

Section: Introductionmentioning

confidence: 99%

Regulation of MET-mediated proliferation of thyroid carcinoma cells by miR-449b

2015

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Thyroid carcinoma (TC) is a lethal cancer worldwide, whereas its carcinogenesis is not fully understood. Although growing evidence has demonstrated that dysregulation of microRNAs (miRNAs) contributes to the development of various cancers, the role of miRNAs in the pathogenesis of TC is poorly characterized. Here, we analyzed the levels of miR-449b in TC tissues and detected significantly lower miR-449b levels in TC tissues. Moreover, the low miR-449b levels were associated with poor survival. We then overexpressed miR-449b by miRNA mimic transfection and inhibited miR-449b by miRNA antisense transfection. Cell growth was analyzed by CCK-8 assay and MTT assay, and apoptosis and cell proliferation were analyzed by flow cytometry. Overexpression of miR-449b significantly inhibited cell growth, while depletion of miR-449b increased cell growth. Moreover, the effects of miR-449b on cell growth were through modulation of cell proliferation rather than through modulation of cell apoptosis. Targeted genes were predicted by a bioinformatics algorithm and confirmed by a dual luciferase reporter assay, showing that miR-449b binds to the 3'-UTR of MET (hepatocyte growth factor receptor) mRNA, to inhibit its expression in TC cells. MET levels were regulated by miR-449b in TT cells. Together, we show that reduced miR-449b levels in TT tissues may promote TC growth, through MET-mediated cell proliferation.

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Section: Introductionmentioning

confidence: 99%

Regulation of MET-mediated proliferation of thyroid carcinoma cells by miR-449b

2015

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“…Specific miRNAs have been found to be differentially expressed in the majority of tumor cases, suggesting that miRNA expression patterns are capable of distinguishing between malignant and normal tissues [134,135]. There is increasing evidence to show that tumor-derived circulating miRNAs have diagnostic or prognostic potential because of their remarkable stability in blood and their characteristic expression in cancers [136][137][138].…”

Section: Mir-100 In Cancer Diagnosis and Prognosismentioning

confidence: 99%

Multiple Roles of MicroRNA-100 in Human Cancer and its Therapeutic Potential

Li¹,

Gao²,

Zhang³

et al. 2015

Cell Physiol Biochem

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MicroRNAs (miRNAs) are a recently discovered class of endogenous, small (about 22 nucleotides) non-coding RNAs, which play important roles in cancer development and progression. Emerging evidence shows that microRNAs exert their regulatory effects by directly binding to the 3'- untranslated regions (UTRs) of their target genes. MicroRNA-100 (miR-100) is aberrantly expressed and functions in many human cancers by regulating multiple cell processes, such as cell cycle, proliferation, differentiation, migration, invasion and apoptosis, via post-transcriptionally regulating various target genes. A better understanding of the molecular mechanisms involved in miR-100-mediated tumor progression will provide an opportunity for exploring novel miR-100-based targeted therapies for human cancers. This review aims to summarize the recently published literature on the roles of miR-100 in regulating tumorigenesis, and explore its potential clinical applications for cancer diagnosis, prognosis and clinical treatment.

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“…MET is an oncogene protein with tyrosine kinase activity, and is also known as hepatocyte growth factor receptor (HGFR) [7], which is a unique receptor for mitogenic factor HGF [8]. After protein translation, the primary single chain MET precursor is cleaved to form alpha and beta subunits, which reunite to form the mature receptor through disulfide molecules [8].…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-3666 Regulates Thyroid Carcinoma Cell Proliferation via MET

Wang

Cai

Chen³

2016

Cell Physiol Biochem

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Background/Aims: Thyroid carcinoma (TC) is a highly lethal malignant cancer and its carcinogenesis remains undetermined. Dysregulation of microRNAs (miRNAs) is well known to be involved in the development of various cancers, including TC, whereas a role of miR-3666 in the pathogenesis of TC has not been appreciated. Methods: We analyzed the levels of MET and miR-3666 in TC tissue and the relationship of miR-3666 levels with patients' prognosis. We then overexpressed miR-3666 by miRNA mimics transfection and inhibited miR-3666 by miRNA antisense transfection in TC cells. Cell survival and growth were analyzed by CCK-8 assay and MTT assay, respectively. Cell apoptosis and proliferation were analyzed by flow cytometry. Bioinformatics analyses were applied to predict miR-3666 targets, which was then confirmed using luciferase reporter assay. Results: We detected significantly higher levels of MET, and significantly lower levels of miR-3666 in TC tissue, compared to the adjacent non-tumor tissue. Moreover, the low miR-3666 levels were associated with poor survival of the patients. Overexpression of miR-3666 significantly inhibited cell growth, while depletion of miR-3666 increased cell growth in TC cells. Moreover, the effects of miR-3666 on cell growth appeared to result from alteration in cell proliferation, rather than changes in cell apoptosis. MiR-3666 was found to bind to the 3'-UTR of MET mRNA to inhibit its translation in TC cells. Conclusion: Reduced miR-3666 levels in TC tissue may promotes TC growth, possibly through MET-mediated cell proliferation.

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MicroRNA-409-3p Functions as a Tumor Suppressor in Human Lung Adenocarcinoma by Targeting c-Met

Cited by 50 publications

References 31 publications

Regulation of MET-mediated proliferation of thyroid carcinoma cells by miR-449b

Regulation of MET-mediated proliferation of thyroid carcinoma cells by miR-449b

Multiple Roles of MicroRNA-100 in Human Cancer and its Therapeutic Potential

MicroRNA-3666 Regulates Thyroid Carcinoma Cell Proliferation via MET

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