miR-506 attenuates methylation of lncRNA MEG3 to inhibit migration and invasion of breast cancer cell lines via targeting SP1 and SP3

Wang, Xinxing; Guo, Guangcheng; Qian, Xin; Dou, Dongwei; Zhang, Zhe; Xu, Xiaodong; Duan, Xin; Pei, Xinhong

doi:10.1186/s12935-018-0642-8

Cited by 32 publications

(29 citation statements)

References 34 publications

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“…Our data shows that, in the absence of CCDC26, genome is hypomethylated which leads to increase in apoptosis and DNA damage, and cell growth inhibition. In the past, non-coding RNAs have been shown to impact DNA methylation levels through transcriptional and post-transcriptional regulation of DNMT genes Wang, Guo, et al 2018;Cheng et al 2018;Mohammad et al 2010;Di Ruscio et al 2013;Merry et al 2015). However, unlike many previous publications, DNMT expression levels were unchanged in CCDC26 KOs, indicating that the mechanism behind the observed DNA hypomethylation is different.…”

Section: Discussionmentioning

confidence: 70%

A long intergenic non-coding RNA regulates nuclear localisation of DNA methyl transferase-1

Jones

Wijesinghe

Halsall

et al. 2020

Preprint

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DNA methyl-transferase-1 or DNMT1 maintains DNA methylation in the genome and is important for regulating gene expression in cells. Aberrant changes in DNMT1 activity are observed in many diseases. Therefore, understanding the mechanisms behind alteration of DNMT1 activity is important. Here, we show that CCDC26, a nuclear long non-coding RNA frequently mutated in myeloid leukaemia, directly interacts with DNMT1. In the absence of CCDC26 RNA, DNMT1 is mis-located in the cytoplasm. As a result, genomic DNA is significantly hypomethylated, which is accompanied by a slower cell growth rate and increased cell death. These results point

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Section: Discussionmentioning

confidence: 70%

A long intergenic non-coding RNA regulates nuclear localisation of DNA methyl transferase-1

Jones

Wijesinghe

Halsall

et al. 2020

Preprint

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“…Silencing DNMT1 inhibits the proliferation, migration and invasion of breast cancer cells by promoting the expression of MEG3 through demethylation Current studies have found that lncRNA MEG3 is regulated by DNMT1, and the promoter of MEG3 is methylated under the in uence of DNMT1, while MEG3 appears to be hypermethylated and lowly expressed in tumors 9,15,17 . We further examined the effect of the interaction of MEG3 and DNMT1 on the breast cancer cells.…”

Section: Resultsmentioning

confidence: 99%

“…Aberrant methylation promoted by DNMT1 can increase the drug resistance of breast cancer cells to anticancer drugs. DNMT1 also promotes the development of breast cancer by reducing the expression of MEG3 9 . Therefore, this study veri ed the role of DNMT1 in regulating MEG3, and the results were consistent with previous reports.…”

Section: Discussionmentioning

confidence: 99%

“…The downregulation of DNMT1 has been reported to inhibit the proliferation and invasion of breast cancer cells 8 . DNMT1 can downregulate maternally expressed gene 3 (MEG3) expression through increasing methylation level of MEG3 in breast cancer 9 . MEG3 has been identi ed as an imprinted gene with maternal expression and encodes a long non-coding RNA (lncRNA) 10 .…”

Section: Introductionmentioning

confidence: 99%

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DNMT1 facilitates proliferation and metastasis of breast cancer cells by promoting MEG3 promoter methylation in MEG3/miR-494-3p/OTUD4 regulatory axis

Zhu

Wang

et al. 2020

Preprint

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Background To explore the mechanism of DNMT1 facilitating proliferation and metastasis of breast cancer cells by promoting MEG3 promoter methylation in MEG3/miR-494-3p/OTUD4 regulatory axis. Methods Human breast cancer cell lines (MCF-7, MDA-MB-231, SKBR3) and human breast epithelial cell line MCF10A were selected for the experiments. The expressions of DNMT1, MEG3, miR-494-3p and OTUD4 were detected by qRT-PCR. Western blot was used to detect the protein expressions of DNMT1 and OTUD4. ChIP assay verified the binding relationship of DNMT1 and MEG3 promoter region. MEG3 methylation and its level were test by MethPrimer software and MSP, respectively. The targeted binding sites of miR-494-3p and MEG3/OTUD4 were predicted by bioinformatics. RIP and dual-luciferase reporter gene assays verified the combination of miR-494-3p and MEG3/OTUD4. Cell proliferation, migration and invasion abilities were detected by CCK-8, wound healing and Transwell assays. Results DNMT1 was highly expressed while MEG3 was poorly expressed in breast cancer cells. Silencing DNMT1 inhibited the proliferation, migration and invasion of breast cancer cells by promoting the expression of lncRNA MEG3 through demethylation. MEG3 as a ceRNA regulated the expression of miR-494-3p in breast cancer. In addition, miR-494-3p could bind to the 3’-UTR of OTUD4, thus negatively regulating the expression of OTUD4 and forming the MEG3/miR-494-3p/OTUD4 regulatory axis that affected the proliferation, invasion and migration of breast cancer. Overexpression of MEG3 could inhibit breast cancer tumor growth in vivo. Conclusion Silencing DNMT1 promoted the expression of MEG3 through demethylation, which inhibited the expression of miR-494-3p to promote the expression of downstream target OTUD4, thus inhibiting the proliferation, migration and invasion abilities of breast cancer cells.

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“…3 In recent years, the incidence of breast cancer is increasing. [4][5][6] However, the pathogenesis of breast cancer remains unclear. 7 Accumulating evidence have shown that lncRNAs exert important roles in the progression of breast cancer.…”

Section: Introductionmentioning

confidence: 99%

<p>lncRNA PART1 Promotes Breast Cancer Cell Progression by Directly Targeting miR-4516</p>

Wang

2020

CMAR

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Introduction: Breast cancer is a serious threat to human health. It is meaningful to study the pathogenesis of breast cancer. lncRNAs have been found to play vital roles in numerous biological processes including development, immunology and cancer. Methods: qRT-PCR was performed to examine the expressions of PART1 and miR-4516. CCK-8 assay, colony formation assay and transwell assay were used to examine the progression of breast cancer cells. Results: In this study, we showed that lncRNA PART1 was highly expressed in breast cancer cells. Knockdown of PART1 induced decreased proliferation, invasion and migration of breast cancer cells. Moreover, we found that PART1 can bind to miR-4516 directly. We also found that inhibition of miR-4516 could rescue the decreased proliferation, migration and invasion of breast cancer cells induced by knockdown of PART1. Discussion: lncRNA PART1 and miR-4516 were proven to be involved in the progression of many cancers. However, the roles of lncRNA PART1 and miR-4516 in the regulation of breast cancer remain unknown. Here, we demonstrated that PART1 can bind to miR-4516 to decrease the expression of miR-4516 and promote the development of breast cancer.

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miR-506 attenuates methylation of lncRNA MEG3 to inhibit migration and invasion of breast cancer cell lines via targeting SP1 and SP3

Cited by 32 publications

References 34 publications

A long intergenic non-coding RNA regulates nuclear localisation of DNA methyl transferase-1

A long intergenic non-coding RNA regulates nuclear localisation of DNA methyl transferase-1

DNMT1 facilitates proliferation and metastasis of breast cancer cells by promoting MEG3 promoter methylation in MEG3/miR-494-3p/OTUD4 regulatory axis

<p>lncRNA PART1 Promotes Breast Cancer Cell Progression by Directly Targeting miR-4516</p>

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