MiR-217 promoted the proliferation and invasion of glioblastoma by repressing YWHAG

Wang, Hongbin; Zhi, Hua; Ma, Dongzhou; Li, Tao

doi:10.1016/j.cyto.2016.12.013

Cited by 32 publications

(16 citation statements)

References 35 publications

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“…5e-f and Supplementary 13b-f) 21,39 . In BARBEKO screen, perturbations in p53 signaling pathway showed strong impact on cell proliferation, in agreement with prior reports, including p53 negative regulators MDM2, MDM4 and UBE2N [55][56][57] being essential for cell viability, positive regulator USP28 58 and p53's downstream effector retinoblastoma protein (RB1) 59 restricting persistent cell proliferation. Unexpectedly, we noticed one sgRNA Stop targeting the C-terminus of cyclin-dependent kinase inhibitor 1A (CDKN1A, encoding p21) was drastically depleted ( Supplementary Fig.…”

Section: Disruptions In the C-terminus Of Cdkn1a Caused Cell Deathsupporting

confidence: 90%

Genome-wide interrogation of gene functions through base editor screens empowered by barcoded sgRNAs

Liu

et al. 2020

Preprint

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Canonical CRISPR screens rely on Cas9-induced DNA double-strand breaks (DSBs) to generate targeted gene knockouts. These DSB-dependent methodologies may yield false-positive results by mistakenly assuming targeted loci as essential for cell viability, especially when high-copy-number sites are targeted. Here, we use CRISPR cytosine base editors for genome-scale knockout screens by perturbing gene start codons or splice sites, or by introducing premature termination codons (PTCs). Combining with iBAR strategy we have previously established, we realized an iBARed cytosine Base Editing-mediated gene KnockOut (BARBEKO) screening strategy at a genome-scale (targeting 17,501 genes) in multiple human cell lines. By constructing such a cell library through lentiviral infection at a high MOI (up to 10), we significantly reduced starting cells while producing screening results with improved efficiency and accuracy. More importantly, in comparison with Cas9-mediated cell fitness screens, BARBEKO screens are no longer affected by DNA-cleavage induced cytotoxicity in HeLa, K562, or DSB-sensitive RPE1 cells. We anticipate that BARBEKO offers a valuable tool to complement the current CRISPR screens in various settings.

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Section: Disruptions In the C-terminus Of Cdkn1a Caused Cell Deathsupporting

confidence: 90%

Genome-wide interrogation of gene functions through base editor screens empowered by barcoded sgRNAs

Liu

et al. 2020

Preprint

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“…5C), suggesting a functional role of miR-628-3p in MYCN gene expression. Finally, our analysis identified a set of differentially expressed miRNAs, such as miR-130b-5p, miR-217, miR-3065-3p and miR-3182, known as oncomiRs in several other tumours (64–67), but whose role in NB has not yet been investigated (Table V). Notably, miR-130b and miR-301b belong to the same genomic cluster located on chromosome 22 and are significantly upregulated in triple-negative (lacking the expression of the oestrogen receptor, the progesterone receptor and the human epidermal growth factor receptor 2) breast cancer (64), having a direct role in cyclin G2 regulation.…”

Section: Resultsmentioning

confidence: 99%

A sketch of known and novel MYCN-associated miRNA networks in neuroblastoma

et al. 2017

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Neuroblastoma (NB) originates from neural crest-derived precursors and represents the most common childhood extracranial solid tumour. MicroRNAs (miRNAs), a class of small non-coding RNAs that participate in a wide variety of biological processes by regulating gene expression, appear to play an essential role within the NB context. High-throughput next generation sequencing (NGS) was applied to study the miRNA transcriptome in a cohort of NB tumours with and without MYCN-amplification (MNA and MNnA, respectively) and in dorsal root ganglia (DRG), as a control. Out of the 128 miRNAs differentially expressed in the NB vs. DRG comparison, 47 were expressed at higher levels, while 81 were expressed at lower levels in the NB tumours. We also found that 23 miRNAs were differentially expressed in NB with or without MYCN-amplification, with 17 miRNAs being upregulated and 6 being downregulated in the MNA subtypes. Functional annotation analysis of the target genes of these differentially expressed miRNAs demonstrated that many mRNAs were involved in cancer-related pathways, such as DNA-repair and apoptosis as well as FGFR and EGFR signalling. In particular, we found that miR-628-3p negatively affects MYCN gene expression. Furthermore, we identified a novel miRNA candidate with variable expression in MNA vs. MNnA tumours, whose putative target genes are implicated in the mTOR pathway. The present study provides further insight into the molecular mechanisms that correlate miRNA dysregulation to NB development and progression.

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“…Mesci et al suggested that miR-330-3p promotes the metastasis of human BC by targeting collagen and calcium binding EGF domains 1 (14). Another study by Wang et al (15) indicated that miR-217 promotes the proliferation and invasion of BC by repressing tyrosine 3-monooxygenase/tryptophan 5-monooxygenase activation protein-γ. miR-3677 correlates significantly with the survival time of patients with hepatocellular carcinoma (16)(17)(18).…”

Section: Introductionmentioning

confidence: 99%

Targeting of TLE3 by miR‑3677 in human breast cancer promotes cell proliferation, migration and invasion

et al. 2019

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Numerous studies have indicated an important function of microRNAs (miRs) in breast cancer (BC) progression, oncogenesis and metastasis. However, the function of miR-3677, which has been revealed to be upregulated in BC [The Cancer Genome Atlas (TCGA) data], has not been investigated to date. In the present study, miR-3677 was revealed to be upregulated in BC as determined using TCGA. miR-3677 was significantly upregulated in BC tissues and cell lines compared with those noted in adjacent non-cancerous tissues and primary normal breast cells (P<0.05). The overexpression of miR-3677 promoted the cell proliferation, migration and invasion of BC cells. Using bioinformatics algorithms and luciferase assays, a novel target gene for miR-3677, namely transducin-like enhancer of Split3 (TLE3), was identified. Silencing of TLE3 in miR-3677-transfected BC cells suppressed their proliferation and migration. An inverse correlation was observed between miR-3677 and TLE3 expression levels in human BC tissues. In conclusion, the present study demonstrated that miR-3677 promoted BC cell proliferation, migration and invasion by inhibiting TLE3 expression, which provided a novel mechanism and a promising therapeutic target for patients with BC.

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MiR-217 promoted the proliferation and invasion of glioblastoma by repressing YWHAG

Cited by 32 publications

References 35 publications

Genome-wide interrogation of gene functions through base editor screens empowered by barcoded sgRNAs

Genome-wide interrogation of gene functions through base editor screens empowered by barcoded sgRNAs

A sketch of known and novel MYCN-associated miRNA networks in neuroblastoma

Targeting of TLE3 by miR‑3677 in human breast cancer promotes cell proliferation, migration and invasion

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