Long noncoding MAGI2‐AS3 promotes colorectal cancer progression through regulating miR‐3163/TMEM106B axis

Ren, Hui; Li, Zhi; Zheng-jun, Tang; Li, Jun; Lang, Xiaoou

doi:10.1002/jcp.29360

Cited by 49 publications

(39 citation statements)

References 33 publications

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“…This sequence is composed of a set of complex structural variants (Fig 1d) and overlaps with the MAGI2. Various somatic genetic alterations in this gene are observed in ovarian, breast and colorectal carcinomas [6][7][8].…”

Section: Resultsmentioning

confidence: 99%

A new long-read dog assembly uncovers thousands of exons and functional elements missing in the previous reference

Wang

Wallerman

Arendt

et al. 2020

Preprint

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AbstractHere we present a new high-quality canine reference genome with gap number reduced 41-fold, from 23,836 to 585. Analysis of existing and novel data, RNA-seq, miRNA-seq and ATAC-seq, revealed a large proportion of these harboured previously hidden elements, including genes, promoters and miRNAs. Short-read dark regions were detected, and genomic regions completed, including the DLA, TCR and 366 cancer genes. 10x sequencing of 27 dogs uncovered a total of 22.1 million SNPs, Indels and larger structural variants (SVs). 1.4% overlap with protein coding genes and could provide a source of normal or aberrant phenotypic modifications.

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Section: Resultsmentioning

confidence: 99%

A new long-read dog assembly uncovers thousands of exons and functional elements missing in the previous reference

Wang

Wallerman

Arendt

et al. 2020

Preprint

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“…Kundu et al declared that TMEM106B played a positive role in lung cancer metastasis [26]. Ren et al disclosed that TMEM106B could reverse the promotional role in cell apoptosis and the suppressive roles in cell proliferation and migration in CRC cells mediated by MAGI2-AS3 silencing via acting as a target of miR-3163, indicating that TEME106B might play a positive role in CRC progression [18]. Herein, TMEM106B expression was inversely modulated by miR-488-3p and TMEM106B upregulation restored the impacts of miR-488-3p overexpression on CRC cell growth, cell cycle, apoptosis and metastasis.…”

Section: Discussionmentioning

confidence: 99%

“…Nevertheless, the effects of miR-488-3p in CRC are not fully understood. In CRC, Ren et al have pointed out that transmembrane protein 106B (TMEM106B) can be targeted by miR-3163 to participate in the progression of CRC [18]. Nonetheless, whether miR-488-5p can target TMEM106B to take part in CRC development has not been documented yet.…”

Section: Introductionmentioning

confidence: 99%

CircSEC24A promotes colorectal cancer progression by regulating miR-488-3p/TMEM106B axis

Hu¹,

Peng²,

Cao³

2020

Preprint

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Background: Currently, more and more circular RNAs (circRNAs) have been identified to exert their functions in tumor progression, including colorectal cancer (CRC). However, the role of circSEC24A (circ_0003528) in CRC remains unknown.Methods: Quantitative real-time polymerase chain reaction (qRT-PCR) was conducted to determine the levels of circSEC24A, SEC24A and microRNA-488-3p (miR-488-3p). The characterization of circSEC24A was investigated by Actinomycin D and RNase R digestion assays. 3-(4, 5-dimethyl-2-thiazolyl)-2, 5-diphenyl-2-H-tetrazolium bromide (MTT) assay was used to assess cell proliferation. Flow cytometry analysis was adopted for cell apoptosis and cell cycle process. Transwell assay was employed to evaluate cell migration and invasion. Western blot assay was performed to determine protein levels. Dual-luciferase reporter assay was utilized to explore the relationship between miR-488-3p and circSEC24A or transmembrane protein 106B (TMEM106B). Murine xenograft model was constructed to explore the effect of circSEC24A in vivo .Results: CircSEC24A level was increased in CRC tissues and cells. CircSEC24A deficiency impeded cell proliferation, cell cycle process, migration and invasion and induced apoptosis in CRC cells in vitro and blocked tumorigenesis in vivo . MiR-488-3p was a target of circSEC24A and miR-488-3p was downregulated in CRC tissues and cells. The inhibitory effect of circSEC24A silencing on CRC cell progression was restored by miR-488-3p inhibition. Moreover, TMEM106B could be negatively regulated by miR-488-3p via acting as a downstream gene of miR-488-3p. MiR-488-3p overexpression decelerated CRC cell progression by targeting TMEM106B.Conclusion: CircSEC24A facilitated CRC progression by regulating miR-488-3p/TMEM106B axis, which might provide a promising treatment approach for CRC.

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“…On the other hand, overexpression of MAGI2-AS3 has been explained to straighten tumor progression by absorbing miR-141/200a and consequently, up-regulate ZEB1 in the gastric cancer cells [34]. In addition, MAGI2-AS3 up-regulation has been shown to exacerbated CRC proliferation and migration by modulating miR-3163 through upregulating TMEM106B [35]. LncRNA NEAT1 is a prominent lncRNA that has been described in a variety of cancers [36].…”

Section: Kaplan-meier Survival Analysis Of Differentially Expressed Gmentioning

confidence: 99%

Comprehensive Analysis of LncRNAs Role in Tumorigenesis of Colon Adenocarcinoma

Poursheikhani¹,

Abbaszadegan²,

Nokhandani³

et al. 2020

Preprint

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Background Colon adenocarcinoma (COAD) is one of the most common gastrointestinal cancers globally. Molecular aberrations of tumor suppressors and/or oncogenes are the main contributors to its tumorigenesis. However, the exact underlying mechanisms of COAD pathogenesis are not clear yet. Thus, there is an urgent need to indicate promising potential diagnostic and prognostic biomarkers in COAD patients. In the current study, level 3 RNA-seq and miR-seq data and corresponding clinical data of colon adenocarcinoma (COAD) were retrieved from the TCGA database.The “limma” package in R software was utilized to indicate the differentially expressed genes. For in silico functional analysis, GO and KEGG signaling pathways were conducted. PPI network was constructed based on the STRING online database by Cytoscape 3.7.2. A ceRNA network was also constructed by “GDCRNATools” package in R software. Kaplan-Meier survival analysis (log-rank test) was used to indicate the relation between RNA expressions with patient’s survival time.Results The differential expression data demonstrated that 1512 mRNAs, 188 lncRNAs, and 329 miRNAs were differentially expressed in COAD. The GO and KEGG pathway analysis indicated that the differentially expressed mRNAs were primarily enriched in canonical processes in cancer. The PPI network showed that the PPARGC1A, ADAMTS5, PTGS2, FGFR2, TBX1, TWIST1, KIT, BDNF and MET proteins were the critical hubs. The Kaplan-Meier analysis revealed that 128 mRNAs, 15 lncRNAs, and 39 miRNAs were associated with overall survival time in the patients. The ceRNA network data demonstrated that three lncRNA including MAGI2-AS3, NEAT1, and SNHG3 genes were involved in the development of COAD.Conclusions Altogether, we integrated differentially expressed mRNAs, lncRNAs, and miRNAs in COAD bioinformatically. Our data suggested promising lncRNAs in the diagnosis and prognosis of patients with COAD.

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Long noncoding MAGI2‐AS3 promotes colorectal cancer progression through regulating miR‐3163/TMEM106B axis

Cited by 49 publications

References 33 publications

A new long-read dog assembly uncovers thousands of exons and functional elements missing in the previous reference

A new long-read dog assembly uncovers thousands of exons and functional elements missing in the previous reference

CircSEC24A promotes colorectal cancer progression by regulating miR-488-3p/TMEM106B axis

Comprehensive Analysis of LncRNAs Role in Tumorigenesis of Colon Adenocarcinoma

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