scholarly journals Retraction: ‘Genistein mediated histone acetylation and demethylation activates tumor suppressor genes in prostate cancer cells’ by Nobuyuki Kikuno, Hiroaki Shiina, Shinji Urakami, Ken Kawamoto, Hiroshi Hirata, Yuichiro Tanaka, Shahana Majid, Mikio Igawa and Rajvir Dahiya

2017 ◽  
Vol 141 (7) ◽  
pp. 1492-1492
Keyword(s):  
Prostate Cancer ◽  
Tumor Suppressor ◽  
Histone Acetylation ◽  
Cancer Cells ◽  
Tumor Suppressor Genes ◽  
Prostate Cancer Cells ◽  
Suppressor Genes

Retracted: Genistein mediated histone acetylation and demethylation activates tumor suppressor genes in prostate cancer cells

2008 ◽  
Vol 123 (3) ◽  
pp. 552-560 ◽  
Author(s):  
Nobuyuki Kikuno ◽  
Hiroaki Shiina ◽  
Shinji Urakami ◽  
Ken Kawamoto ◽  
Hiroshi Hirata ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Tumor Suppressor ◽  
Histone Acetylation ◽  
Cancer Cells ◽  
Tumor Suppressor Genes ◽  
Prostate Cancer Cells ◽  
Suppressor Genes

scholarly journals Activation of silenced tumor suppressor genes in prostate cancer cells by a novel energy restriction-mimetic agent

The Prostate ◽  
2012 ◽  
Vol 72 (16) ◽  
pp. 1767-1778 ◽  
Author(s):  
Hsiang-Yu Lin ◽  
Yi-Chiu Kuo ◽  
Yu-I Weng ◽  
I-Lu Lai ◽  
Tim H.-M. Huang ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Tumor Suppressor ◽  
Cancer Cells ◽  
Tumor Suppressor Genes ◽  
Energy Restriction ◽  
Prostate Cancer Cells ◽  
Suppressor Genes

GENISTEIN MEDIATED HISTONE ACETYLATION AND DEMETHYLATION ACTIVATE TUMOR SUPPRESSOR GENES IN PROSTATE CANCER

2008 ◽  
Vol 179 (4S) ◽  
pp. 45-45
Author(s):  
Nobuyuki Kikuno ◽  
Hiroaki Shiina ◽  
Shinji Urakami ◽  
Ken Kawamoto ◽  
Hiroshi Hirata ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Tumor Suppressor ◽  
Histone Acetylation ◽  
Tumor Suppressor Genes ◽  
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 Crosstalk between Prostate Cancer Cells and Tumor-Associated Fibroblasts Enhances the Malignancy by Inhibiting the Tumor Suppressor PLZF

Cancers ◽  
2020 ◽  
Vol 12 (5) ◽  
pp. 1083
Author(s):  
Kum Hee Noh ◽  
Ae Jin Jeong ◽  
Haeri Lee ◽  
Song-Hee Lee ◽  
Eunhee Yi ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Tumor Suppressor ◽  
Tumor Growth ◽  
Cancer Cells ◽  
Cancer Metastasis ◽  
Tyrosine Phosphatase ◽  
Migration And Invasion ◽  
Metastatic Progression ◽  
Prostate Cancer Cells ◽  
Prostate Cancer Metastasis

Although prostate cancer is clinically manageable during the early stages of progression, metastatic progression severely compromises the prognosis and leads to mortality. Constitutive activation of STAT3 has been connected to prostate cancer malignancy, and abolishing the STAT3 activity may diminish tumor growth and metastasis. However, its suppressor genes and pathways have not been well established. In this study, we show that promyelocytic leukemia zinc finger (PLZF) has a putative tumor-suppressor function in prostate cancer by inhibiting phosphorylation of STAT3. Compared with a benign prostate, high-grade prostate cancer patient tissue was negatively correlated with PLZF expression. PLZF depletion accelerated proliferation and survival, migration, and invasion in human prostate cancer cells. Mechanistically, we demonstrated a novel role of PLZF as the transcriptional regulator of the tyrosine phosphatase SHP-1 that inhibits the oncogenic JAKs–STAT3 pathway. These results suggest that the collapse of PLZF expression by the CCL3 derived from fibroblasts accelerates the cell migration and invasion properties of prostate cancer cells. Our results suggest that increasing PLZF could be an attractive strategy for suppressing prostate cancer metastasis as well as for tumor growth.

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.

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