scholarly journals Emodin enhances the demethylation by 5-Aza-CdR of pancreatic cancer cell tumor-suppressor genes P16, RASSF1A and ppENK

2016 ◽  
Vol 35 (4) ◽  
pp. 1941-1949 ◽  
Author(s):  
FENG-PING PAN ◽  
HONG-KUN ZHOU ◽  
HE-QI BU ◽  
ZI-QIANG CHEN ◽  
HAO ZHANG ◽  
...  
2014 ◽  
Vol 15 (4) ◽  
pp. 419-427 ◽  
Author(s):  
Masoumeh Azizi ◽  
Ladan Teimoori-Toolabi ◽  
Mohsen Karimi Arzanani ◽  
Kayhan Azadmanesh ◽  
Pezhman Fard-Esfahani ◽  
...  

2020 ◽  
Author(s):  
Heying Zhang ◽  
Juan Zeng ◽  
Yuexian Li ◽  
Cheng Sun ◽  
Yang Zhou ◽  
...  

Abstract Objective: To construct a key prognosis-related regulatory network and to identify the epigenomic alterations of RNAs that have crucial functions in cancer pathogenesis.Methods: RNA expression profiles of miRNAs, mRNAs and circRNAs were extracted from the NCBI GEO and EBI ArrayExpress databases. The identification of differentially expressed genes was performed by R language. Databases such as starBase and TCGA were used for annotation, visualization, and integrated discovery. GO and KEGG pathway enrichment analyses were performed by DAVID 6.8. The key prognosis-related regulatory network was constructed with Cytoscape software. The involved circRNAs were verified by quantitative real-time PCR (qRT-PCR) in five pancreatic cancer cell lines. Proliferation ability was assessed by the CCK-8 assay, apoptosis was detected by flow cytometry, and migratory and invasive abilities were assessed by Transwell assays.Results: In total, 798 differentially expressed genes, consisting of 85 circRNAs, 19 miRNAs and 694 mRNAs, were obtained. A miRNA interaction network was predicted and used to construct a prognosis-related regulatory network. GO annotation and KEGG pathway analysis revealed important biological processes and pathways in pancreatic cancers. The key regulatory factors in the network were miR-146b-5p and miR-152. Eight circRNAs included in the network were verified, and hsa_circ_0006502 was downregulated in the five tested pancreatic cancer cell lines and functioned as a tumor suppressor, as predicted.Conclusion: In conclusion, a key prognosis-related regulatory network in pancreatic cancers was constructed through bioinformatics analysis of public RNA databases, and miR-146b-5p and miR-152 were the key regulatory factors. Hsa_circ_0006502 was identified as a tumor suppressor that interacted closely with miR-146b-5p and might serve as a potential therapeutic agent.


2000 ◽  
Vol 118 (4) ◽  
pp. A46
Author(s):  
Takashi Ueki ◽  
Minoru Toyota ◽  
Kimberly M. Walter ◽  
Elizabeth Jaffee ◽  
Charles J. Yeo ◽  
...  

1995 ◽  
Vol 23 (5) ◽  
pp. 293-300 ◽  
Author(s):  
M.-O. Grimm ◽  
B. J�rgens ◽  
W. A. Schulz ◽  
K. Decken ◽  
D. Makri ◽  
...  

Author(s):  
Michelle Maurin ◽  
Devin J. Jones ◽  
Mik A. Black ◽  
Justin Y. Newberg ◽  
Nancy A. Jenkins ◽  
...  

2019 ◽  
Vol 12 ◽  
pp. 251686571983901 ◽  
Author(s):  
Shahad A Qadi ◽  
Mohammed A Hassan ◽  
Ryan A Sheikh ◽  
Othman AS Baothman ◽  
Mazin A Zamzami ◽  
...  

The epigenetic silencing of tumor suppressor genes (TSGs) is a common finding in several solid and hematological tumors involving various epigenetic readers and writers leading to enhanced cell proliferation and defective apoptosis. Thymoquinone (TQ), the major biologically active compound of black seed oil, has demonstrated anticancer activities in various tumors by targeting several pathways. However, its effects on the epigenetic code of cancer cells are largely unknown. In the present study, we performed RNA sequencing to investigate the anticancer mechanisms of TQ-treated T-cell acute lymphoblastic leukemia cell line (Jurkat cells) and examined gene expression using different tools. We found that many key epigenetic players, including ubiquitin-like containing plant homeodomain (PHD) and really interesting new gene (RING) finger domains 1 ( UHRF1), DNMT1,3A,3B, G9A, HDAC1,4,9, KDM1B, and KMT2A,B,C,D,E, were downregulated in TQ-treated Jurkat cells. Interestingly, several TSGs, such as DLC1, PPARG, ST7, FOXO6, TET2, CYP1B1, SALL4, and DDIT3, known to be epigenetically silenced in various tumors, including acute leukemia, were upregulated, along with the upregulation of several downstream pro-apoptotic genes, such as RASL11B, RASD1, GNG3, BAD, and BIK. Data obtained from RNA sequencing were confirmed using quantitative reverse transcription polymerase chain reaction (RT-qPCR) in Jurkat cells, as well as in a human breast cancer cell line (MDA-MB-468 cells). We found that the decrease in cell proliferation and in the expression of UHRF1, DNMT1, G9a, and HDAC1 genes in both cancer cell (Jurkat cells and MDA-MB-468 cells) lines depends on the TQ dose. Our results indicate that the use of TQ as an epigenetic drug represents a promising strategy for epigenetic therapy for both solid and blood tumors by targeting both DNA methylation and histone post-translational modifications.


2016 ◽  
Vol 4 (1) ◽  
pp. 115-120 ◽  
Author(s):  
Huacheng He ◽  
Diego Altomare ◽  
Ufuk Ozer ◽  
Hanwen Xu ◽  
Kim Creek ◽  
...  

A polymer/copper combination selectively kills cancer cells by targeting their high glutathione level, upregulated oncogenes, and downregulated tumor suppressor genes.


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