Global analysis of H3K27me3 as an epigenetic marker in prostate cancer progression

Ngollo, Marjolaine; Lebert, André; Daures, Marine; Judes, Gaëlle; Rifaï, Khaldoun; Dubois, Lucas; Kémény, Jean-Louis; Penault‐Llorca, Frédérique; Bignon, Yves‐Jean; Guy, Laurent; Bernard‐Gallon, Dominique

doi:10.1186/s12885-017-3256-y

Cited by 89 publications

(63 citation statements)

References 33 publications

(33 reference statements)

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“…Local recurrence and distant metastasis are the major patterns of treatment failure in NPC. Most cancers are caused by accumulation of genomic or epigenetic alterations [ 19 – 24 ], and epigenetic alterations play an important role in the development of NPC [ 9 , 25 ]. Several studies have indicated that aberrantly methylated genes could serve as prognostic biomarkers for NPC [ 26 – 28 ].…”

Section: Discussionmentioning

confidence: 99%

Epigenetic mediated zinc finger protein 671 downregulation promotes cell proliferation and tumorigenicity in nasopharyngeal carcinoma by inhibiting cell cycle arrest

Zhang

Wen

Liu

et al. 2017

J Exp Clin Cancer Res

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BackgroundEpigenetic abnormalities play important roles in nasopharyngeal cancer (NPC), however, the epigenetic changes associated with abnormal cell proliferation remain unclear.MethodsWe detected epigenetic change of ZNF671 in NPC tissues and cell lines by bisulfite pyrosequencing. We evaluated zinc finger protein 671 (ZNF671) expression in NPC cell lines and clinical tissues using real-time PCR and western blotting. Then, we established NPC cell lines that stably overexpressed ZNF671 and knocked down ZNF671 expression to explore its function in NPC in vitro and in vivo. Additionally, we investigated the potential mechanism of ZNF671 by identifying the mitotic spindle and G2/M checkpoint pathways pathway downstream genes using gene set enrichment analysis, flow cytometry and western blotting.Results ZNF671 was hypermethylated in NPC tissues and cell lines. The mRNA and protein expression of ZNF671 was down-regulated in NPC tissues and cell lines and the mRNA expression could be upregulated after the demethylation agent 5-aza-2′-deoxycytidine treatment. Overexpression of ZNF671 suppressed NPC cell proliferation and colony formation in vitro; silencing ZNF671 using a siRNA had the opposite effects. Additionally, overexpression of ZNF671 reduced the tumorigenicity of NPC cells in xenograft model in vivo. The mechanism study determined that overexpressing ZNF671 induced S phase arrest in NPC cells by upregulating p21 and downregulating cyclin D1 and c-myc.ConclusionsEpigenetic mediated zinc finger protein 671 downregulation promotes cell proliferation and enhances tumorigenicity by inhibiting cell cycle arrest in NPC, which may represent a novel potential therapeutic target.Electronic supplementary materialThe online version of this article (10.1186/s13046-017-0621-2) contains supplementary material, which is available to authorized users.

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Section: Discussionmentioning

confidence: 99%

Epigenetic mediated zinc finger protein 671 downregulation promotes cell proliferation and tumorigenicity in nasopharyngeal carcinoma by inhibiting cell cycle arrest

Zhang

Wen

Liu

et al. 2017

J Exp Clin Cancer Res

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“…Research by Ngollo et al Showed that GRID2 interacts with H3K27me3 in prostate cancer and is signi cantly overexpressed. [30] The protein encoded by ATG4D belongs to the ATG4 mammalian family (four cysteine proteases, ATG4A4D class), which is closely related to autophagosome maturation and apoptosis pathways [31]. Gil et al's research shows that ATG4D can play a role as a tumor suppressor in the development of colorectal cancer [32].…”

Section: Discussionmentioning

confidence: 99%

Identification and Validation of an Individualized Autophagy-Clinical Prognostic Index in Gastric Cancer Patients

Qiu

Sun

Wang

et al. 2020

Preprint

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Background : The purpose of this study is to perform bioinformatics analysis of autophagy-related genes in gastric cancer, and to construct a multi-gene joint signature for predicting the prognosis of gastric cancer. Methods : GO and KEGG analysis were applied for differentially expressed autophagy-related genes in gastric cancer, and PPI network was constructed in Cytoscape software. In order to optimize the prognosis evaluation system of gastric cancer, we established a prognosis model integrating autophagy-related genes. We used single factor Cox proportional risk regression analysis to screen genes related to prognosis from 204 autophagy-related genes in The Atlas Cancer Genome (TCGA) gastric cancer cohort. Then, the generated genes were applied to the Least Absolute Shrinkage and Selection Operator (LASSO). Finally, the selected genes were further included in the multivariate Cox proportional hazard regression analysis to establish the prognosis model. According to the median risk score, patients were divided into high-risk group and low-risk group, and survival analysis was conducted to evaluate the prognostic value of risk score. Finally, by combining clinic-pathological features and prognostic gene signatures, a nomogram was established to predict individual survival probability. Results : GO analysis showed that the 28 differently expressed autophagy-related genes was enriched in cell growth, neuron death, and regulation of cell growth. KEGG analysis showed that the 28 differently expressed autophagy-related genes were related to platinum drug resistance, apoptosis and p53 signaling pathway. The risk score was constructed based on 4 genes (GRID2, ATG4D,GABARAPL2, CXCR4), and gastric cancer patients were significantly divided into high-risk and low-risk groups according to overall survival. In multivariate Cox regression analysis, risk score was still an independent prognostic factor (HR = 1.922, 95% CI = 1.573-2.349, P < 0.001). Cumulative curve showed that the survival time of patients with low-risk score was significantly longer than that of patients with high-risk score (P < 0.001). The external data GSE62254 proved that nomograph had a great ability to evaluate the prognosis of individual gastric cancer patients. Conclusions: This study provides a potential prognostic marker for predicting the prognosis of GC patients and the molecular biology of GC autophagy.

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“…Treatment failure in NPC is usually due to local recurrence and distant metastasis (24). Recent studies have reported that epigenetic alterations play an important role in the initiation and development of most cancers (25)(26)(27)(28), including NPC (10,29). Several studies have also reported that aberrantly methylated genes may serve as prognostic biomarkers (30)(31)(32).…”

Section: Discussionmentioning

confidence: 99%

Hypermethylation of SHISA3 Promotes Nasopharyngeal Carcinoma Metastasis by Reducing SGSM1 Stability

Zhang

Guo

et al. 2019

Cancer Research

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Altered DNA methylation is a key feature of cancer, and aberrant methylation is important in nasopharyngeal carcinoma (NPC) development. However, the methylation mechanisms underlying metastasis of NPC remain unclear. Analyzing data from public databases and conducting our own experiments, we report here that promoter hypermethylation of SHISA3 is common and contributes to the downregulation of this gene in many types of tumors, including NPC. SHISA3 suppressed NPC cell invasion and metastasis in vitro and in vivo by impeding the E3 ubiquitin ligase tripartite motif containing 21 (TRIM21)-mediated ubiquitination and degradation small G protein signaling modulator 1 (SGSM1) and by inhibiting the MAPK pathway activation. Silencing SGSM1 abrogated the inhibitory effect of SHISA3 on NPC cell migration and invasion. This newly identified SHISA3-TRIM21-SGSM1 axis could be a novel therapeutic target in NPC.Significance: These findings highlight the mechanism by which a newly identified tumor suppressor SHISA3 suppresses invasion and metastasis of nasopharyngeal carcinoma. Migration and invasion assaysCells (5 Â 10 4 or 1 Â 10 5 ) suspended in 200 mL of serum-free medium were plated into transwell chambers (8-mm pores, Corning) precoated with (migration assay) or without (invasion assay) Matrigel (BD Biosciences) cultured at 37 C for 12 hours or 24 hours. The cells attached to the bottom surface of the insert filter were fixed with methyl alcohol, stained with crystal violet, and counted in 10 random fields of view per well. Cell viability assayCells (1 Â 10 3 ) were seeded into 96-well plates and incubated for indicated time periods (1, 2, 3, 4, and 5 days). On the indicated days, CCK-8 (10 mL; Dojindo) were added per well following incubation for 2 hours, and the 450 nm absorbance of each well was read on a spectrophotometer. Colony formation assayCells (0.3 Â 10 3 ) were seeded into 6-well plates and cultured for 1 week (CNE2 cells) or 2 weeks (SUNE1 cells). The colonies were quantified after fixation with methyl alcohol and stained with crystal violet.

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Global analysis of H3K27me3 as an epigenetic marker in prostate cancer progression

Cited by 89 publications

References 33 publications

Epigenetic mediated zinc finger protein 671 downregulation promotes cell proliferation and tumorigenicity in nasopharyngeal carcinoma by inhibiting cell cycle arrest

Epigenetic mediated zinc finger protein 671 downregulation promotes cell proliferation and tumorigenicity in nasopharyngeal carcinoma by inhibiting cell cycle arrest

Identification and Validation of an Individualized Autophagy-Clinical Prognostic Index in Gastric Cancer Patients

Hypermethylation of SHISA3 Promotes Nasopharyngeal Carcinoma Metastasis by Reducing SGSM1 Stability

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