MiR-541-3p reverses cancer progression by directly targeting TGIF2 in non-small cell lung cancer

Lu, Youjin; Liu, Rong‐Yu; Hu, Ke; Wang, Ying

doi:10.1007/s13277-016-5241-5

Cited by 35 publications

(31 citation statements)

References 24 publications

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“…Another study revealed that miR-541 is involved in regulating vascular smooth muscle cell proliferation [19]. In the present study, our results indicating that miR-541 expression is decreased in SCLC are consistent with the findings by Lu [18]. In addition, the finding that miR-541 is a tumor suppressor in both breast cancer and SCLC makes miR-541 potentially valuable in the clinical treatment of human tumor diseases.…”

Section: Discussionsupporting

confidence: 92%

miR‐541 suppresses proliferation and invasion of squamous cell lung carcinoma cell lines via directly targeting high‐mobility group AT‐hook 2

et al. 2018

Cancer Medicine

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An increasing number of studies have demonstrated that micro‐ribonucleic acids (miRNAs) are important tumor suppressors during carcinogenesis. However, the function of miRNA‐541 (miR‐541) in malignancies, especially lung cancer, has not been widely reported. In this study, miR‐541 expression was significantly decreased in squamous cell lung carcinoma (SCLC) cancerous tissue and SCLC cell lines. To analyze miR‐541 function in SCLC, we overexpressed miR‐541 in SCLC cell lines (SK‐MES‐1 and H226). According to the CCK8, wound scratch, and transwell invasion assay results, miR‐541 overexpression significantly inhibited SCLC cell proliferation, migration, and invasion ability. Next, using RT‐PCR, Western blotting, immunocytochemistry, and luciferase assays, HMGA2 was identified, for the first time, as a direct regulatory target of miR‐541 in SK‐MES‐1 and H226 cells. Furthermore, upregulating HMGA2 expression significantly alleviated the suppressive effects of miR‐541 on SK‐MES‐1 and H226 cell proliferation, migration, and invasion. In summary, our study revealed that miR‐541 inhibited SCLC proliferation and invasion by directly targeting HMGA2.

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Section: Discussionsupporting

confidence: 92%

miR‐541 suppresses proliferation and invasion of squamous cell lung carcinoma cell lines via directly targeting high‐mobility group AT‐hook 2

et al. 2018

Cancer Medicine

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“…Since our study reports TGIF2 as a novel miR‐490‐3p target not reported so far in any cancer, thus we considered it for downstream functional analysis. Literature so far suggests the dual nature of TGIF2 where it may function as a tumor suppressor or as an oncogene . Also, in line with our observation, TGIF2 was shown to promote aggressive phenotype in gliomas .…”

Section: Discussionsupporting

confidence: 89%

Polycomb complex mediated epigenetic reprogramming alters TGF‐β signaling via a novel EZH2/miR‐490/TGIF2 axis thereby inducing migration and EMT potential in glioblastomas

Vinchure

Sharma

Tabasum

et al. 2019

Intl Journal of Cancer

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Recent advancement in understanding cancer etiology has highlighted epigenetic deregulation as an important phenomenon leading to poor prognosis in glioblastoma (GBM). Polycomb repressive complex 2 (PRC2) is one such important epigenetic modifier reportedly altered in GBM. However, its defined mechanism in tumorigenesis still remains elusive. In present study, we analyzed our in‐house ChIPseq data for H3k27me3 modified miRNAs and identified miR‐490‐3p to be the most common target in GBM with significantly downregulated expression in glioma patients in both TCGA and GBM patient cohort. Our functional analysis delineates for the first time, a central role of PRC2 catalytic unit EZH2 in directly regulating expression of this miRNA and its host gene CHRM2 in GBM. In accordance, cell line treatment with EZH2 siRNA and 5‐azacytidine also confirmed its coregulation by CpG and histone methylation based epigenetic mechanisms. Furthermore, induced overexpression of miR‐490‐3p in GBM cell lines significantly inhibited key hallmarks including cellular proliferation, colony formation and spheroid formation, as well as epithelial‐to‐mesenchymal transition (EMT), with downregulation of multiple EMT transcription factors and promigratory genes (MMP9, CCL5, PIK3R1, ICAM1, ADAM17 and NOTCH1). We also for the first time report TGFBR1 and TGIF2 as two direct downstream effector targets of miR‐490‐3p that are also deregulated in GBM. TGIF2, a novel target, was shown to promote migration and EMT that could partially be rescued by miR‐490‐3p overexpression. Overall, this stands as a first study that provides a direct link between epigenetic modulator EZH2 and oncogenic TGF‐β signaling involving novel miR‐490‐3p/TGIF2/TGFBR1 axis, that being targetable might be promising in developing new therapeutic intervention strategies for GBM.

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“…Upregulation of eca‐miR‐493b and eca‐miR‐541 was associated with advanced tumour stage (ESA) in ES tumours and might therefore also be of prognostic significance. Interestingly, these miRNAs possess rather tumour‐suppressive functions in diverse human cancers where they are often downregulated . If upregulation of eca‐miR‐493b and eca‐miR‐541 drives oncogenesis in ES and whether inhibition of these two miRNAs could possibly stop ES disease progression, needs to be further investigated.…”

Section: Discussionmentioning

confidence: 99%

Differentially expressed microRNAs, including a large microRNA cluster on chromosome 24, are associated with equine sarcoid and squamous cell carcinoma

Bogedale

Jagannathan

Gerber

et al. 2019

Vet Comparative Oncology

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The aim of this study was to investigate microRNA (miRNA) differential expression in the two most common equine skin tumours, equine sarcoid (ES) and squamous cell carcinoma (SCC), and its potential influence on the tumour microenvironment at post‐transcriptional level. We investigated miRNA fingerprints in four subgroups: mild (ESM) and aggressive (ESA) ES and ocular SCC (oSCC) and genital SCC (gSCC). Three tumours and three control samples were included in each of the four subgroups. Following next generation sequencing, miRNA differential expression analysis using DESeq2 was carried out. Pathways associated with the human mature homologues of identified dysregulated miRNAs were predicted using DIANA‐ miRPath v3.0. When comparing tumour vs control tissue, 57 miRNAs in ESM, six in ESA, 47 in oSCC and zero in gSCC were found to be differentially expressed and may thus serve as potential diagnostic tissue biomarkers. Whereas, ES lesions in general were associated with downregulation of the miR‐200 family, which may trigger epithelial‐mesenchymal transition, ESM lesions were associated with upregulation of the proposed tumour‐suppressive miRNA cluster on equine chromosome 24. In contrast, the oSCC tumours showed downregulation of this cluster as well as downregulation of the miR‐34 family, which may favour oSCC tumour cell metabolism. To further validate the proposed diagnostic miRNA fingerprints and their suggested biological effects, further miRNA studies need to be carried out in larger study cohorts.

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MiR-541-3p reverses cancer progression by directly targeting TGIF2 in non-small cell lung cancer

Cited by 35 publications

References 24 publications

miR‐541 suppresses proliferation and invasion of squamous cell lung carcinoma cell lines via directly targeting high‐mobility group AT‐hook 2

miR‐541 suppresses proliferation and invasion of squamous cell lung carcinoma cell lines via directly targeting high‐mobility group AT‐hook 2

Polycomb complex mediated epigenetic reprogramming alters TGF‐β signaling via a novel EZH2/miR‐490/TGIF2 axis thereby inducing migration and EMT potential in glioblastomas

Differentially expressed microRNAs, including a large microRNA cluster on chromosome 24, are associated with equine sarcoid and squamous cell carcinoma

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