MALAT1 modulates the autophagy of retinoblastoma cell through miR‐124‐mediated stx17 regulation

Huang, Jun; Yang, Yuting; Fang, Fang; Liu, Ke

doi:10.1002/jcb.26464

Cited by 81 publications

(49 citation statements)

References 46 publications

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“…36,37 Moreover, lncRNAs seemed to penetrate into all aspects of gene regulation, including epigenetic inheritance, transcription, post-transcription and translation. 38,39 Interestingly, Jun Huang et al 40 reported that lncRNA MALAT1 mediated autophagy of retinoblastoma cells through acting on miR-124. Alternatively, lncRNA H19 inhibited progression of retinoblastoma cells via offsetting the action of miR-17-92 cluster, 41 and lncRNA CCAT1 negatively regulated miR-218-5p to facilitate the proliferation and growth of SO-RB50 and Y79 cell lines.…”

Section: Discussionmentioning

confidence: 99%

LncRNA HOTAIR/miR‐613/c‐met axis modulated epithelial‐mesenchymal transition of retinoblastoma cells

Yang

et al. 2018

J Cellular Molecular Medi

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Since lncRNAs could modulate neoplastic development by modulating downstream miRNAs and genes, this study was carried out to figure out the synthetic contribution of HOTAIR, miR‐613 and c‐met to viability, apoptosis and proliferation of retinoblastoma cells. Totally 276 retinoblastoma tissues and tumour‐adjacent tissues were collected, and human retinoblastoma cell lines (ie, Y79, HXO‐Rb44, SO‐Rb50 and WERI‐RB1) were also gathered. Moreover, transfections of pcDNA3.1‐HOTAIR, si‐HOTAIR, miR‐613 mimic, miR‐613 inhibitor, pcDNA3.1/c‐met were performed to evaluate the influence of HOTAIR, miR‐613 and c‐met on viability, apoptosis and epithelial‐mesenchymal transition (EMT) of retinoblastoma cells. Dual‐luciferase reporter gene assay was also arranged to confirm the targeted relationship between HOTAIR and miR‐613, as well as between miR‐613 and c‐met. Consequently, up‐regulated HOTAIR and down‐regulated miR‐613 expressions displayed associations with poor survival status of retinoblastoma patients (P < 0.05). Besides, inhibited HOTAIR and promoted miR‐613 elevated E‐cadherin expression, yet decreased Snail and Vimentin expressions (P < 0.05). Simultaneously, cell proliferation and cell viability were also less‐motivated (P < 0.05). Nonetheless, c‐met prohibited the functioning of miR‐613, resulting in promoted cell proliferation and viability, along with inhibited cell apoptosis (P < 0.05). Finally, HOTAIR was verified to directly target miR‐613, and c‐met was the direct target gene of miR‐613 (P < 0.05). In conclusion, the role of lncRNA HOTAIR/miR‐613/c‐met signalling axis in modulating retinoblastoma cells’ viability, apoptosis and expressions of EMT‐specific proteins might provide evidences for developing appropriate diagnostic and treatment strategies for retinoblastoma.

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Section: Discussionmentioning

confidence: 99%

LncRNA HOTAIR/miR‐613/c‐met axis modulated epithelial‐mesenchymal transition of retinoblastoma cells

Yang

et al. 2018

J Cellular Molecular Medi

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“…Metastasis associated lung adenocarcinoma transcript 1 (MALAT‐1) interacts with SR proteins and is located on nuclear speckles close to the spliceosome machinery (Tripathi et al, ; Wilusz, ). Downregulation of lncRNA MALAT‐1 is related to reduced cell proliferation in vitro (J. Huang, Yang, Fang, & Liu, ). In ovarian cancer, it associates with regulatory splice protein RNA‐binding protein fox‐1 homolg 2 (RBFOX2).…”

Section: Splicing Alterations In Cancermentioning

confidence: 99%

Splicing and cancer: Challenges and opportunities

2019

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Constitutive splicing is favored in strong splice sites, which have the conserved consensus sequences at 5 0 (CAG|GUAAGU) and 3 0 (NYAG|G) splice sites. Exons are usually shorter sequences, ranging from 50 to 250 bp, whereas introns can have broader length variation, from <100 bp to more than 1,000 bp, and around 20% of human introns are larger than 5 kb (Lander et al., 2001). In addition to constitutive exon splicing, the presence of alternative splice sites leads to variable ways to mature an mRNA ( Figure 2). Exons and introns might host alternative splice sites, which are similar to, but usually not as strong as, consensus splice sites (Fu & Ares, 2014;Kornblihtt et al., 2013). If a 5 0 or 3 0 alternative site lies within an exon, part of this exon might be read as an intron. Also, alternative splicing can lead to exon skipping, in which a constitutive 3 0 splice site fails to be recognized and assembly of spliceosome proceeds to the next available 3 0 splice site, which can result in exclusion of an exon. Alternatively, 5 0 splice sites might not be read as well, resulting in intron retention. In some transcripts, a mutual exclusion of exons might take place generating different messages . Cryptic splice sites are similar to consensus sites, but they are usually recognized only after a mutation in the gene, or of a spliceosome component, leading to alterations in the final message. In breast cancer, mutations in splicing factor 3B subunit 1 (SF3B1), for example, induce the use of cryptic 3 0 splice sites (DeBoever et al., 2015). Single nucleotide variants (SNVs) of 1,812 tumor samples were analyzed by whole-exome sequencing and revealed exon skipping and intron retention were among the most frequently observed alternative splicing events (Jung et al., 2015; Box 1).Alternative splicing mechanisms are dependent on recognition of splice site sequences in the pre-mRNA, which in turn depends on both the strength of sequences as well as the presence of proteins and signals that guide the spliceosome to these regions. Alternative exons in humans and mice are surrounded by more conserved regulatory sequences than constitutive exons, indicating the former ones are under strict regulation. Consistently, 30-50% of ISEs are located nearby alternative exons (Yeo, Van Nostrand, & Liang, 2007). Interestingly, ISEs and ESSs show a positional overlap in different pre-mRNA substrates, indicating the regulation depends on their positioning with respect to the 5 0 upstream exon and the bound proteins (Y. Wang et al., 2012). The ISSs can interfere with exon inclusion in different pre-mRNAs, and regulate 5 0 splice site choice, therefore, exerting alternative splicing regulation (Y. Wang et al., 2013). In this sense, mutations in exonic and intronic sequences are critical and might affect the balance of regulatory sequences and also their activity, since most effects in splicing are location-dependent. Intronic mutations are commonly associated with nonsense-mediated decay responses, caused by an increased rate of premature stop ...

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“…Researchers found lncRNA‐MALAT1 was robustly induced by hypoxia in several cancer cell types . In addition, several studies reported that lncRNA‐MALAT1 modulates the activity of autophagy . More importantly, recent research indicated expression of lncRNA‐MALAT1 was significantly increased in the ectopic endometrium of patients with ovarian endometriosis .…”

Section: Introductionmentioning

confidence: 99%

Long non‐coding RNA MALAT1 mediates hypoxia‐induced pro‐survival autophagy of endometrial stromal cells in endometriosis

Liu

Zhang

Xiong

et al. 2018

J Cellular Molecular Medi

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Endometriosis is a common gynecological disease characterized by diminished apoptosis, sustained ectopic survival of dysfunctional endometrial cells. Hypoxia has been implicated as a crucial microenvironmental factor that contributes to endometriosis. It has been reported that long non‐coding RNA MALAT1 (lncRNA‐MALAT1) highly expressed in endometriosis and up‐regulated by hypoxia. Hypoxia may also induce autophagy, which might act as cell protective mechanism. However, the relationship between lncRNA‐MALAT1 and autophagy under hypoxia conditions in endometriosis remains unknown. In the present study, we found that both lncRNA‐MALAT1 and autophagy level were up‐regulated in ectopic endometrium from patients with endometriosis, and its expression level correlates positively with that of hypoxia‐inducible factor‐1α (HIF‐1α). In cultured human endometrial stromal cells, both lncRNA‐MALAT1 and autophagy were induced by hypoxia in a time‐dependent manner and lncRNA‐MALAT1 up‐regulation was dependent on HIF‐1α signalling. Our analyses also show that knockdown of lncRNA‐MALAT1 suppressed hypoxia induced autophagy. Furthermore, inhibiting autophagy with specific inhibitor 3‐Methyladenine (3‐MA) and Beclin1 siRNA enhanced apoptosis of human endometrial stromal cells under hypoxia condition. Collectively, our findings identify that lncRNA‐MALAT1 mediates hypoxia‐induced pro‐survival autophagy of endometrial stromal cells in endometriosis.

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MALAT1 modulates the autophagy of retinoblastoma cell through miR‐124‐mediated stx17 regulation

Cited by 81 publications

References 46 publications

LncRNA HOTAIR/miR‐613/c‐met axis modulated epithelial‐mesenchymal transition of retinoblastoma cells

LncRNA HOTAIR/miR‐613/c‐met axis modulated epithelial‐mesenchymal transition of retinoblastoma cells

Splicing and cancer: Challenges and opportunities

Long non‐coding RNA MALAT1 mediates hypoxia‐induced pro‐survival autophagy of endometrial stromal cells in endometriosis

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