Epigenetic Mechanisms of LncRNAs Binding to Protein in Carcinogenesis

Shin, Teo Jeon; Lee, Kanghoon; Cho, Je‐Yoel

doi:10.3390/cancers12102925

Cited by 23 publications

(21 citation statements)

References 132 publications

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“…LncRNA can crosstalk with chromatin, DNA, RNA, and proteins, regulating GC cell progression via transcriptional and posttranscriptional mechanisms ( Kong et al, 2018 ; Zhuo et al, 2019 ). The cellular distribution of lncRNAs is informative for lncRNA functions ( Shin et al, 2020 ). A large number of lncRNAs function by binding to a protein partner ( Castello et al, 2016 ; Chen, 2016 ).…”

Section: Discussionmentioning

confidence: 99%

p53-Induced LINC00893 Regulates RBFOX2 Stability to Suppress Gastric Cancer Progression

Zhou

et al. 2022

Front. Cell Dev. Biol.

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Long noncoding RNAs (lncRNAs) have been reported to regulate diverse tumorigenic processes. However, little is known about long intergenic non-protein coding RNA 00893 (LINC00893) and its role in gastric cancer (GC). Herein we investigated its biological functions and molecular mechanism in GC. LINC00893 was decreased in GC tissues but significantly elevated in AGS cells after treatment with Nutlin-3. In GC patients, it was found that low expression of LINC00893 was correlated with tumor growth, metastasis and poor survival. Functionally, overexpression of LINC00893 suppressed the proliferation, migration and invasion of GC cells. Mechanistically, LINC00893 regulated the expression of epithelial-mesenchymal transition (EMT)-related proteins by binding to RNA binding fox-1 homolog 2 (RBFOX2) and promoting its ubiquitin-mediated degradation, thus suppressing the EMT and related functions of GC. In addition, the transcription factor p53 can regulate the expression of LINC00893 in an indirect way. Taken together, these results suggested that LINC00893 regulated by p53 repressed GC proliferation, migration and invasion by functioning as a binding site for RBFOX2 to regulate its stability and the expression of EMT-related proteins. LINC00893 acts as a tumor-inhibiting lncRNA that is induced by p53 in GC and regulates EMT by binding to RBFOX2, thus providing a novel experimental basis for the clinical treatment of GC.

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Section: Discussionmentioning

confidence: 99%

p53-Induced LINC00893 Regulates RBFOX2 Stability to Suppress Gastric Cancer Progression

Zhou

et al. 2022

Front. Cell Dev. Biol.

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“…To clarify the mechanism by which HOTAIRM1 regulates the malignant phenotype of tMSCs, subcellular localization of HOTAIRM1 was detected by qRT-PCR. The results showed that HOTAIRM1 was mainly existed in nucleus (Figures 3(a) - 3(b) ) which indicated that HOTAIRM1 plays regulatory roles via recruiting RNA-binding proteins (RBPs) [ 27 , 28 ]. Next, starBase was used to search the RBPs to which HOTAIRM1 could bind, and five RBPs were screened out.…”

Section: Resultsmentioning

confidence: 99%

HOTAIRM1 Maintained the Malignant Phenotype of tMSCs Transformed by GSCs via E2F7 by Binding to FUS

Liu

Zhou

Dong

et al. 2022

Journal of Oncology

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Objective. Mesenchymal stromal/stem cells (MSCs) are an important part of the glioma microenvironment and are involved in the malignant progression of glioma. In our previous study, we showed that MSCs can be induced to a malignant phenotype (tMSCs) by glioma stem cells (GSCs) in the microenvironment. However, the potential mechanism by which tMSCs maintain their malignant phenotype after malignant transformation has not been fully clarified. Methods. The expression of HOTAIRM1, FUS, and E2F7 was detected by qRT-PCR. Clone formation, EdU, and Transwell assay were used to explore the role of HOTAIRM1, FUS, and E2F7 on the proliferation, migration, and invasion of tMSCs. Bioinformatics analysis and RNA immunoprecipitation were used to explore the relation among HOTAIRM1, FUS, and E2F7. Results. HOTAIRM1 was upregulated in tMSCs compared with MSCs. Loss- and gain-of-function assays showed that HOTAIRM1 promoted the proliferation, migration, and invasion of tMSCs. qRT-PCR and functional assays revealed that E2F7 might be the downstream target of HOTAIRM1. A further study of the mechanism showed that HOTAIRM1 could bind to FUS, an RNA-binding protein (RBP), and thus regulate E2F7, which could promote the malignant phenotype of tMSCs. Conclusion. Our study revealed that the HOTAIRM1/FUS/E2F7 axis is involved in the malignant progression of tMSCs transformed by GSCs in the glioma microenvironment and may function as a novel target for glioma therapy.

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“…Epigenetic mechanisms such as histone modifications, DNA methylation, non-coding RNAs and chromatin remodeling were proved to regulate gene expression by many cross talk ways 5 . DNA methylation is one of the most widely studied epigenetic mechanisms, which is a covalent modification of DNA, plays an important role in the regulation of genome function, often occurs in hepatocellular carcinoma, bladder cancer, prostate cancer and many other common cancers 6 .…”

Section: Introductionmentioning

confidence: 99%

Epigenetic silencing of ZIC4 contributes to cancer progression in hepatocellular carcinoma

Chen

Tang

et al. 2020

Cell Death Dis

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Inactivation of tumor suppressor gene played critical roles in the development and progression of human hepatocellular carcinoma (HCC). Zic family member 4 (ZIC4) is transcription factor and plays an important role in the developmental process. However, the expression and biological role of ZIC4 in HCC is poorly understood. Here, bioinformatics analysis based on The Cancer Genome Atlas (TCGA) database revealed an aberrant hypermethylation of ZIC4 in HCC. ZIC4 is frequently hypermethylated in promoter region and down expressed in HCC cells and tissues. Functionally, ZIC4 inhibition facilitated the proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT) in vitro and in vivo. Conversely, ZIC4 overexpression reduced proliferation and invasiveness of HCC cells. In addition, ZIC4 inhibition rescued the antitumor effect induced by enhancer of zeste homolog 2 (EZH2) knockdown or EZH2 inhibitor. Mechanistically, EZH2 knockdown or EZH2 inhibitor reduced the enrichment of EZH2 and H3K27me3 in ZIC4 promoter region and leading to the upregulation of ZIC4. Altogether, these data indicate that epigenetic silencing of ZIC4 by EZH2 mediated H3K27me3 is an important mechanism in HCC and provide a new therapeutic target for the treatment of hepatocellular carcinoma disease.

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Epigenetic Mechanisms of LncRNAs Binding to Protein in Carcinogenesis

Cited by 23 publications

References 132 publications

p53-Induced LINC00893 Regulates RBFOX2 Stability to Suppress Gastric Cancer Progression

p53-Induced LINC00893 Regulates RBFOX2 Stability to Suppress Gastric Cancer Progression

HOTAIRM1 Maintained the Malignant Phenotype of tMSCs Transformed by GSCs via E2F7 by Binding to FUS

Epigenetic silencing of ZIC4 contributes to cancer progression in hepatocellular carcinoma

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