scholarly journals Peperomin E reactivates silenced tumor suppressor genes in lung cancer cells by inhibition of DNA methyltransferase

2016 ◽  
Vol 107 (10) ◽  
pp. 1506-1519 ◽  
Author(s):  
Xin‐zhi Wang ◽  
Ying Cheng ◽  
Kui‐long Wang ◽  
Rui Liu ◽  
Xiao‐lin Yang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Tumor Suppressor ◽  
Cancer Cells ◽  
Tumor Suppressor Genes ◽  
Dna Methyltransferase ◽  
Lung Cancer Cells ◽  
Suppressor Genes

Up-regulation of tumor suppressor genes might promote the malignant phenotype of cancer cells

2007 ◽  
Vol 69 (6) ◽  
pp. 1379 ◽  
Author(s):  
Liu Hong ◽  
Xiaohua Li ◽  
Haifeng Jin ◽  
Li Yan ◽  
Kaichun Wu ◽  
...  
Keyword(s):  
Tumor Suppressor ◽  
Cancer Cells ◽  
Tumor Suppressor Genes ◽  
Malignant Phenotype ◽  
Suppressor Genes

scholarly journals Targeting DNA methylation for treating triple-negative breast cancer

2019 ◽  
Vol 20 (16) ◽  
pp. 1151-1157 ◽  
Author(s):  
Jia Yu ◽  
Jacqueline Zayas ◽  
Bo Qin ◽  
Liewei Wang
Keyword(s):  
Breast Cancer ◽  
Dna Methylation ◽  
Tumor Suppressor ◽  
Triple Negative Breast Cancer ◽  
Targeted Therapies ◽  
Tumor Suppressor Genes ◽  
Dna Methyltransferase ◽  
Triple Negative ◽  
Suppressor Genes ◽  
Dna Methyltransferase Inhibitors

Triple-negative breast cancer (TNBC) accounts for 15–20% of all invasive breast cancers and tends to have aggressive histological features and poor clinical outcomes. Unlike, estrogen receptor- or HER2-positive diseases, TNBC patients currently lack the US FDA-approved targeted therapies. DNA methylation is a critical mechanism of epigenetic modification. It is well known that aberrant DNA methylation contributes to the malignant transformation of cells by silencing critical tumor suppressor genes. DNA methyltransferase inhibitors reactivate silenced tumor suppressor genes and result in tumor growth arrest, with therapeutic effects observed in patients with hematologic malignancies. The antitumor effect of these DNA methyltransferase inhibitors has also been explored in solid tumors, especially in TNBC that currently lacks targeted therapies.

scholarly journals Thymoquinone-Induced Reactivation of Tumor Suppressor Genes in Cancer Cells Involves Epigenetic Mechanisms

2019 ◽  
Vol 12 ◽  
pp. 251686571983901 ◽  
Author(s):  
Shahad A Qadi ◽  
Mohammed A Hassan ◽  
Ryan A Sheikh ◽  
Othman AS Baothman ◽  
Mazin A Zamzami ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Tumor Suppressor ◽  
Cancer Cells ◽  
Cell Line ◽  
Rna Sequencing ◽  
Cancer Cell ◽  
Tumor Suppressor Genes ◽  
Jurkat Cells ◽  
Leukemia Cell Line ◽  
Suppressor Genes

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.

scholarly journals KMT2D inhibits the growth and metastasis of bladder Cancer cells by maintaining the tumor suppressor genes

2019 ◽  
Vol 115 ◽  
pp. 108924 ◽  
Author(s):  
Peng Sun ◽  
Tong Wu ◽  
Xiaoliang Sun ◽  
Zilian Cui ◽  
Haiyang Zhang ◽  
...  
Keyword(s):  
Bladder Cancer ◽  
Tumor Suppressor ◽  
Cancer Cells ◽  
Tumor Suppressor Genes ◽  
Suppressor Genes ◽  
Bladder Cancer Cells
Sign in / Sign up

Export Citation Format

Share Document