scholarly journals Cancer cell-selective killing polymer/copper combination

2016 ◽  
Vol 4 (1) ◽  
pp. 115-120 ◽  
Author(s):  
Huacheng He ◽  
Diego Altomare ◽  
Ufuk Ozer ◽  
Hanwen Xu ◽  
Kim Creek ◽  
...  
Keyword(s):  
Tumor Suppressor ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Tumor Suppressor Genes ◽  
Glutathione Level ◽  
Suppressor Genes

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

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.

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

Inactivation of tumor suppressor genes and deregulation of the c-myc gene in urothelial cancer cell lines

1995 ◽  
Vol 23 (5) ◽  
pp. 293-300 ◽  
Author(s):  
M.-O. Grimm ◽  
B. J�rgens ◽  
W. A. Schulz ◽  
K. Decken ◽  
D. Makri ◽  
...  
Keyword(s):  
Tumor Suppressor ◽  
Cell Lines ◽  
Cancer Cell ◽  
Tumor Suppressor Genes ◽  
Urothelial Cancer ◽  
Cancer Cell Lines ◽  
Suppressor Genes ◽  
Myc Gene ◽  
Urothelial Cancer Cell

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

scholarly journals REVERSAL OF HYPERMETHYLATION AND REACTIVATION OF TUMOR SUPPRESSOR GENES DUE TO NATURAL COMPOUNDS IN BREAST CANCER CELLS

2020 ◽  
Vol 02 (01) ◽  
pp. 63-75
Author(s):  
Debasray Saha ◽  
Neeraj Vaishnav ◽  
Zubiya Ahsan ◽  
Nisha Rani ◽  
Runjhun Mathur ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Tumor Suppressor ◽  
Cancer Cells ◽  
Tumor Suppressor Genes ◽  
Breast Cancer Cells ◽  
Natural Compounds ◽  
Suppressor Genes

scholarly journals HIF-1 — A BIG CHAPTER IN THE CANCER TALE

2016 ◽  
Vol 38 (1) ◽  
pp. 9-12 ◽  
Author(s):  
J Ajdukovic
Keyword(s):  
Tumor Suppressor ◽  
Tumor Progression ◽  
Cancer Cells ◽  
Cancer Progression ◽  
Tumor Suppressor Genes ◽  
Biological Effects ◽  
Hypoxia Inducible Factor ◽  
Signal Molecules ◽  
Suppressor Genes ◽  
Carcinoma Associated Fibroblasts

Approximately 1.0–1.5% of the genome is transcriptionally regulated by hypoxia, and hypoxia-inducible factor (HIF)-1α is the transcription factor modulating many of these genes. Cancer cells are able to survive hypoxic environments and hypoxia itself can activate adaptive cellular responses that contribute to tumor progression. Many HIF-1α-mediated biological effects are beneficial for tumor progression, including metabolic shift toward glycolysis, inhibition of fatty acid β-oxidation, production of cellular reacreactive oxygen species and altering expression of tumor suppressor genes. HIF-1 promotes selective mitochondrial autophagy, resisand altering expression of tumor suppressor genes. HIF-1 promotes selective mitochondrial autophagy, resistance to T cell mediated lysis of cancer cells, induction of pluripotent cancer stem cells, epithelial-mesenchymal and epithelialmesenchymal-endothelial transitions beneficial for tumor growth and progression, loss of E-cadherin. HIF-1 also induces production of signal molecules and cytokines by carcinoma-associated fibroblasts and upregulation of certain microRNAs important for cancer progression. This minireview focuses on the HIF-1 promoting role in tumor initiation and progression and HIF-1 targeting. HIF-1 pathway downregulation seems to be promising in future cancer treatment.

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