LncRNA NEAT1 exacerbates non-small cell lung cancer by upregulating EIF4G2 via miR-582-5p sponging

Zhang, Xin; Sun, Zhonghua; Zou, Yuepei

doi:10.2298/abs200218018z

Cited by 2 publications

(3 citation statements)

References 37 publications

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“…MALAT1 regulated the glucose metabolism of hepatocellular carcinoma cells by enhancing translation of metabolic transcription factor TCF7L2 through mTORC1–4EBP1 axis [ 87 ]. lncRNA NEAT1 represents another example of lncRNAs that contribute to the aggressiveness of non-small cell lung cancer by enhancing eIF4G2 via miR-582-5p sponging effects [ 148 ]. Similarly, lncRNA RP11-284P20.2 enhanced c-met mRNA translation by recruiting eIF3b to c-met and thus promoted proliferation and invasion of hepatocellular carcinoma cells [ 149 ].…”

Section: Acting Mechanisms Of Lncrnas In the Regulation Of Translamentioning

confidence: 99%

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The Role of LncRNAs in Translation

Karakaş

Özpolat

2021

ncRNA

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Long non-coding RNAs (lncRNAs), a group of non-protein coding RNAs with lengths of more than 200 nucleotides, exert their effects by binding to DNA, mRNA, microRNA, and proteins and regulate gene expression at the transcriptional, post-transcriptional, translational, and post-translational levels. Depending on cellular location, lncRNAs are involved in a wide range of cellular functions, including chromatin modification, transcriptional activation, transcriptional interference, scaffolding and regulation of translational machinery. This review highlights recent studies on lncRNAs in the regulation of protein translation by modulating the translational factors (i.e, eIF4E, eIF4G, eIF4A, 4E-BP1, eEF5A) and signaling pathways involved in this process as wells as their potential roles as tumor suppressors or tumor promoters.

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Section: Acting Mechanisms Of Lncrnas In the Regulation Of Translamentioning

confidence: 99%

“… The mechanisms of action of lncRNAs on the regulation of cancer-related protein translation [ 31 , 34 , 35 , 38 , 64 , 67 , 68 , 82 , 84 , 85 , 86 , 87 , 148 , 151 , 153 ]. …”

Section: Figurementioning

confidence: 99%

The Role of LncRNAs in Translation

Karakaş

Özpolat

2021

ncRNA

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“…Zhao et al concluded that downregulation of Neat1 in NSCLC inhibits its growth, migration, and invasion through the miR-204/NUAK1 axis [ 39 ]. Neat1 was further found to affect NSCLC by elevating its malignant potential via the miR-582-5p/EIF4G2 axis [ 40 ]. As we expected, RBM10 overexpression suppressed Neat1 expression, whereas RBM10 silencing promoted Neat1 expression.…”

Section: Discussionmentioning

confidence: 99%

RBM10 regulates alternative splicing of lncRNA Neat1 to inhibit the invasion and metastasis of NSCLC

Cong

et al. 2022

Cancer Cell Int

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Background Non-small cell lung cancer (NSCLC) accounts for more than 85% of the total cases with lung cancer. NSCLC is characterized by easy metastasis, which often spreads to bones, brains and livers. RNA-binding motif protein 10 (RBM10) is an alternative splicing (AS) regulator frequently mutated in NSCLC. We found that there were multiple peak binding sites between RBM10 and long non-coding RNA nuclear enriched abundant transcript 1 (LncRNA Neat1) by crosslinking-immunprecipitation and high-throughput sequencing (Clip-Seq). LncRNA Neat1 plays an indispensable role in promoting cancer in a variety of tumors and produces two splicing variants: Neat1_1 and Neat1_2. This study aims to explore the mechanism of RBM10 and LncRNA Neat1 in invasion and metastasis of NSCLC. Methods Through histological and cytological experiments, we assessed the expression level of RBM10 protein expression. The interaction between RBM10 and Neat1 was evaluated via Clip-Seq and RNA immunoprecipitation assay. The effect of RBM10 on Neat1 and its splicing variants was identified by RT-qPCR. The effect of RBM10 and Neat1 on invasive and metastasis phenotypes of NSCLC was analyzed using transwell invasion assay and scratch test. Additionally, downstream signaling pathway of RBM10 were identified by immunofluorescence and western blot. Results RBM10 exhibited low levels of expression in NSCLC tissues and cells. RBM10 inhibited the invasion and metastasis of NSCLC and recruited Neat1 and Neat1_2. Overexpression of RBM10 simultaneously inhibited Neat1 and Neat1_2, and promoted the expression of Neat1_1. On the other hand, silencing RBM10 promoted Neat1 and Neat1_2, and inhibited the expression of Neat1_1. From this, we concluded that RBM10 regulated AS of Neat1, and the tumor-promoting effect of Neat1 was mainly attributed to Neat1_2. RBM10 had a negative correlation with Neat1_2. In addition, RBM10 upregulated the expression of PTEN and downregulated the phosphorylation of PI3K/AKT/mTOR through Neat1_2, which ultimately inhibited the invasion and metastasis of NSCLC. Conclusion The RBM10 regulated AS of Neat1 to cause the imbalance of Neat1_1 and Neat1_2, and RBM10 suppressed the activation of the PTEN/PI3K/AKT/mTOR signal by downregulating Neat1_2, finally affected the invasion and metastasis of NSCLC.

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LncRNA NEAT1 exacerbates non-small cell lung cancer by upregulating EIF4G2 via miR-582-5p sponging

Cited by 2 publications

References 37 publications

The Role of LncRNAs in Translation

The Role of LncRNAs in Translation

RBM10 regulates alternative splicing of lncRNA Neat1 to inhibit the invasion and metastasis of NSCLC

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