Predicting the Correlation of EZH2 and Cancer Stem Cell Markers in Esophageal Squamous Cell Carcinoma

Madani, GholamReza Karami; Rad, Abolfazl; Molavi, Mehdi; Khales, Sima Ardalan; Abbaszadegan, Mohammad Reza; Forghanifard, Mohammad Mahdi

doi:10.1007/s12029-017-9985-y

Cited by 10 publications

(6 citation statements)

References 28 publications

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“…28 In the current study, EZH2 was significantly upregulated in ESCC cells and tumor tissues, which was consistent with previous research. 29 Knockdown of EZH2 had the same effect on apoptosis and protein expression as overexpression of miR-101-3p. Thus, we hypothesized that miR-101-3 affects apoptosis in ESCC cells by regulating EZH2 expression.…”

Section: Dovepressmentioning

confidence: 93%

<p>LncRNA SNHG6 Inhibits Apoptosis by Regulating EZH2 Expression via the Sponging of MiR-101-3p in Esophageal Squamous-Cell Carcinoma</p>

Wang

Yang

et al. 2020

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Background: The long non-coding RNA (lncRNA) SNHG6 was significantly upregulated in esophageal squamous-cell carcinoma (ESCC), and it promoted ESCC cell proliferation, invasion, and migration. However, the effects of SNHG6 on cell apoptosis and the corresponding underlying mechanisms have not yet reported. Methods: Apoptosis was detected by flow cytometric analysis. Quantitative real-time polymerase chain reaction (qRT-PCR) and Western blotting were used for mRNA and protein quantification, respectively. A luciferase reporter assay was performed to verify downstream target genes for SNHG6 and miR-101-3p. Results: Dysregulation of SNHG6 inhibited apoptosis in ESCC cells and regulated the expression of apoptosis-related proteins such as Bcl-2, Mcl-1, Bax and Caspase-3. Functionally, miR-101-3p could compete binding with 3′-untranslated region of SNHG6 and downregulation of miR-101-3p reversed its effect on cell apoptosis in SNHG6 knockdown cells. EZH2 was confirmed as a downstream target gene of miR-101-3p, silencing EZH2 expression had the same effect on apoptosis and protein expression as knocking down SNHG6. Overexpression of EZH2 reversed the effects of miR-101-3p overexpression on cell apoptosis in ESCC cells. Conclusion: In this study, we found that upregulation of the lncRNA SNHG6 inhibited apoptosis via miR-101-3p/EZH2 axis in ESCC. These findings may contribute to the diagnosis and treatment of ESCC.

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Section: Dovepressmentioning

confidence: 93%

<p>LncRNA SNHG6 Inhibits Apoptosis by Regulating EZH2 Expression via the Sponging of MiR-101-3p in Esophageal Squamous-Cell Carcinoma</p>

Wang

Yang

et al. 2020

OTT

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“…Previous research has demonstrated that EZH2 plays critical roles in the epigenetic silencing of target genes and modulates the proliferation and metastasis of cancer cells (Huqun et al, ; Varambally et al, ). The upregulation of EZH2 has been discovered in many cancer cells, such as non‐small‐cell lung cancer (Huqun et al, ), breast cancer (Chase & Cross, ), esophageal squamous cell carcinoma (Karami Madani et al, ), and colon cancer (Ferraro, Boni, & Pintzas, ). For colon cancer, Ferraro et al (Ferraro et al, ) reported that EZH2 regulated cofilin activity and colon cancer cell migration via targeting integrin α 2 (ITGα 2).…”

Section: Introductionmentioning

confidence: 99%

Retracted: EZH2 regulates H2B phosphorylation and elevates colon cancer cell autophagy

Liu

Yang

Zhong

et al. 2019

Journal Cellular Physiology

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Epigenetic alterations, especially histone modification, play vital roles in the pathogenesis of colon cancer. Upregulation of the enhancer of zeste homolog 2 (EZH2) has been reported to contribute to the initiation and progression of colon cancer. This study analyzed the association between EZH2 and phosphorylation of H2B at tyrosine 37 (H2B Y37ph ) in colon cancer tissues and cells, along with the influences of the EZH2-H2B Y37ph axis on colon cancer cell autophagy. Immunohistochemistry was utilized to assess EZH2 and H2B Y37ph expressions in clinical samples of colon cancer.Cell transfection was carried out to alter EZH2 and H2B Y37ph expressions in colon cancer cells. Co-immunoprecipitation analysis and glutathione-S-transferase (GST) pull down assay were conducted to analyze the association between EZH2 and H2B Y37ph .Western blotting was utilized to measure proteins expressions related to cell autophagy. We found that there was a positive association between EZH2 and H2B Y37ph in colon cancer tissues and cells. EZH2 directly interacted with H2B and promoted H2B Y37ph in colon cancer cells using ATP as a phosphate donor. Moreover, EZH2 levated colon cancer cell autophagy in starvation condition. H2B Y37ph was required for EZH2-elevated colon cancer cell autophagy under starvation condition.The EZH2-H2B Y37ph axis elevated colon cancer cell autophagy possibly via activating transcriptional regulation of ATG genes. In conclusion, EZH2-elevated colon cancer initiation and progression at least in part via inducing colon cancer cell autophagy.EZH2 could phosphorylate H2B Y37 and then induce transcription activation of ATG genes in colon cancer cells under starvation condition. K E Y W O R D SATG genes, cell autophagy, colon cancer, EZH2, histone phosphorylation

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“…revealed that MAGI2-AS3 can down-regulate HOXB7 expression by recruiting EZH2 to initiate the upregulation of H3K27me3 protein expression. As a stemness factor, EZH2 possesses the ability to regulate cell differentiation, embryonic development and cancer development, such that EZH2 silencing demonstrably down-regulates various genes in ESCC (Karami Madani et al, 2018). The indispensable role of H3K27me3 in EZH2-mediated repression of genes in tumorigenesis and tumor progression has also been documented, while expression of H3K27me3 and EZH2 are indicative of poor prognosis of patients with ESCC (Liu et al, 2016).…”

Section: Discussionmentioning

confidence: 99%

“…As a stemness factor, histone methyltransferase EZH2 has the ability to regulate cell differentiation, embryonic development, and cancer development, and EZH2 silencing has been confirmed to downregulate different genes in ESCC (Karami Madani et al, 2018). H3K27me3 is required for EZH2-mediated repression of various genes essential for tumorigenesis and tumor development, while the expression of H3K27me3 and EZH2 could serve as biomarkers in the prediction of ESCC patients' survival and ESCC metastasis (Liu et al, 2016).…”

Section: Magi2-as3 Down-regulates Hoxb7 By Recruiting Ezh2 To Initiatmentioning

confidence: 99%

LncRNA MAGI2-AS3 Overexpression Sensitizes Esophageal Cancer Cells to Irradiation Through Down-Regulation of HOXB7 via EZH2

Cheng

Shi

Lin

et al. 2020

Front. Cell Dev. Biol.

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BackgroundAccumulating evidence has suggested that aberrant expression of long non-coding RNAs (lncRNAs) may contribute to cancer progression in association with radioresistance. The current study aimed to identify the potential role of lncRNA MAGI2-AS3 and the underlying mechanism in its regulation of the radio-sensitivity of esophageal cancer cells.Methods and ResultsInitially, we detected high expression of HOXB7 from microarray-based gene expression profiling of esophageal cancer. Then, we identified the interactions among MAGI2-AS3, HOXB7, and EZH2 by dual-luciferase reporter gene assay, RNA pull-down assay, RIP assay and ChIP assay. HOXB7 was highly-expressed, while MAGI2-AS3 was poorly-expressed in esophageal cancer tissues and cells. The effect of MAGI2-AS3 and HOXB7 on esophageal cancer cell proliferation and apoptosis as well as tumorigenicity of radioresistant cells was examined by gain- and loss-of-function experiments. Interestingly, MAGI2-AS3 down-regulated HOXB7 through interaction with EZH2, which promoted cell apoptosis and inhibited proliferation and radio-resistance. Besides, down-regulation of MAGI2-AS3 exerted a promoting effect on these malignant phenotypes.ConclusionTaken together, our results reveal the potential role of MAGI2-AS3 over-expression in controlling esophageal cancer resistance to radiotherapy by down-regulating HOXB7, this providing a candidate biomarker for resistance to radiotherapy.

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Predicting the Correlation of EZH2 and Cancer Stem Cell Markers in Esophageal Squamous Cell Carcinoma

Abstract: To the best our knowledge, there are variety of small molecule inhibitors to target EZH2 in cancer cells as a treatment candidate; therefore, our data in this study helps the researchers to select EZH2 for cancer therapy based on its mechanism and correlation with other markers.

Cited by 10 publications

References 28 publications

<p>LncRNA SNHG6 Inhibits Apoptosis by Regulating EZH2 Expression via the Sponging of MiR-101-3p in Esophageal Squamous-Cell Carcinoma</p>

<p>LncRNA SNHG6 Inhibits Apoptosis by Regulating EZH2 Expression via the Sponging of MiR-101-3p in Esophageal Squamous-Cell Carcinoma</p>

Retracted: EZH2 regulates H2B phosphorylation and elevates colon cancer cell autophagy

LncRNA MAGI2-AS3 Overexpression Sensitizes Esophageal Cancer Cells to Irradiation Through Down-Regulation of HOXB7 via EZH2

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