Biological and clinical significance of epigenetic silencing of MARVELD1 gene in lung cancer

Shi, Ming; Wang, Shan; Yao, Yuanfei; Li, Yiqun; Zhang, Hao; Han, Fangfang; Nie, Huan; Su, Jie; Wang, Zeyu; Yue, Lei; Cao, Jingyan; Yu, Li

doi:10.1038/srep07545

Cited by 20 publications

(18 citation statements)

References 28 publications

(37 reference statements)

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“…In cancer cells, however, the efficiency of the NMD pathway is often compromised (43,44). Consistently, we found that MDM4-S was readily detectable in melanoma, and inhibition of NMD by cyclohexamide did not lead to a consistent increase in MDM4-S levels (data not shown).…”

Section: Discussionsupporting

confidence: 69%

Antisense oligonucleotide–mediated MDM4 exon 6 skipping impairs tumor growth

Dewaele

Tabaglio

Willekens

et al. 2015

Journal of Clinical Investigation

144

178

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Section: Discussionsupporting

confidence: 69%

Antisense oligonucleotide–mediated MDM4 exon 6 skipping impairs tumor growth

Dewaele

Tabaglio

Willekens

et al. 2015

Journal of Clinical Investigation

144

178

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“…Tumor-related hypomethylation of gene promoter is often linked with aberrant cell proliferation [24, 25]. Our results showed that UPF1 is a potential suppressor in gastric tumor, which holds inhibitory effects on gastric cancer cell proliferation, cell cycle progression and migration.…”

Section: Discussionmentioning

confidence: 72%

The Human RNA Surveillance Factor UPF1 Modulates Gastric Cancer Progression by Targeting Long Non-Coding RNA MALAT1

Li¹,

Geng²,

Ren³

et al. 2017

Cell Physiol Biochem

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Background/Aims: The long non-coding RNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is overexpressed in numerous cancers. However, whether MALAT1 is regulated and the related mechanisms in gastric cancer remain unclear. Methods: Immunohistochemistry and qRT-PCR analyses were used to detect the expression levels of UPF1 and MALAT1 in gastric cancer and adjacent normal tissues. MTT, cell cycle, apoptosis and transwell assays were performed to examine the effects of UPF1 on cell cycle progression, cell proliferation, apoptosis, migration and invasion. Additionally, sodium bisulfate sequencing was used to test the promoter hypermethylation on UPF1 in gastric tumor tissues. Finally, RNA immunoprecipitation and luciferase reporter analyses demonstrated that UPF1 directly bound with MALAT1. Results: The expression of UPF1 was significantly downregulated in gastric cancer and negatively correlated with MALAT1 expression. Patients with lower expression of UPF1 had poorer prognosis than those with higher expression. Overexpression of UPF1 inhibited cell proliferation, cell cycle progression, cell migration and invasion, and promoted cell apoptosis in gastric cancer cells. Moreover, the UPF1-mediated inhibition of gastric cancer progression was reversed by overexpression of MALAT1. A profound downregulation of UPF1 in gastric tumor tissues was due to promoter hypermethylation. Overexpression of UPF1 increased nonsense-mediated mRNA decay (NMD) efficiency and thus led to downregulation of MALAT1. Conclusion: Our results demonstrate that UPF1 is a potential modulator of MALAT1 and that UPF1/MALAT1 pathway could be a therapeutic target for gastric cancer.

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“…They involve a variety of biological processes, including cell cycle progression, chemotactic activity, tight junctions, and clathrin-mediated endocytosis [9,[13][14][15][16] . [10][11] .…”

Section: Discussionmentioning

confidence: 99%

DNMT1 inhibits hepatocellular carcinoma cells by altering the epigenetic modification of Marveld1 gene

Zhang

Luo

Wang

et al. 2020

Preprint

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Objective To study the effect of DNA methyltransferase (DNMT1) on Marveld1 in hepatocellular Carcinoma (HCC), and explore its role in the molecular mechanism of HCC occurrence and development. Methods The expression level of Dnmt1 and Marveld1 genes was detected by RT-PCR in the intraoperative pathological specimens. The human hepatoma Bel7402 and SMMC7721 cell lines down-regulated by DNMT1 gene expression were constructed by SiRNA transfection. The methylation level of Marveld1 promoter region was detected after RT-PCR and West-blot verification. The expression of Marveld1 gene, cell proliferation, invasion and change of cell cycle were detected by RT-PCR and West-blot. The expressions of P53, CyclinD1, P21 and P16 protein were detected by West-blot method. Results The expression of DNMT1 gene in human hepatocarcinoma tissues was higher than that in adjacent tissues. The methylation level of the Marveld1 gene promoter region in human hepatoma cell line down-regulated by DNMT1 gene expression was decreased, the expression level of Marveld1 gene was increased, and the proliferation and invasion ability of cells were weakened. The cell cycle was showed as G1-S phase arrest; P53 and P16 protein expressions were up-regulated, and CyclinD1 and P21 protein expressions were down-regulated. Conclusions Dnmt1 gene is highly expressed in human hepatocarcinoma tissues. Down-regulation of DNMT1 gene expression can decrease the methylation level of Marveld1 promoter region, up-regulate Marveld1 gene and human P53 and P16 proteins expressions, and down-regulate CyclinD1 and P21 proteins expressions, inhibit the proliferation and invasion of human hepatoma cells and can cause cell cycle G1-S arrest.

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Biological and clinical significance of epigenetic silencing of MARVELD1 gene in lung cancer

Cited by 20 publications

References 28 publications

Antisense oligonucleotide–mediated MDM4 exon 6 skipping impairs tumor growth

Antisense oligonucleotide–mediated MDM4 exon 6 skipping impairs tumor growth

The Human RNA Surveillance Factor UPF1 Modulates Gastric Cancer Progression by Targeting Long Non-Coding RNA MALAT1

DNMT1 inhibits hepatocellular carcinoma cells by altering the epigenetic modification of Marveld1 gene

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