scholarly journals The Key Role of E2F in Tumor Suppression through Specific Regulation of Tumor Suppressor Genes in Response to Oncogenic Changes

2018 ◽  
Author(s):  
Kenta Kurayoshi ◽  
Eiko Ozono ◽  
Ritsuko Iwanaga ◽  
Andrew P. Bradford ◽  
Hideyuki Komori ◽  
...  
Keyword(s):  
Tumor Suppressor ◽  
Tumor Suppression ◽  
Tumor Suppressor Genes ◽  
Suppressor Genes ◽  
Specific Regulation

The functional role of tumor suppressor genes in gliomas: Clues for future therapeutic strategies

Neurology ◽  
1998 ◽  
Vol 51 (5) ◽  
pp. 1250-1255 ◽  
Author(s):  
J. Fueyo ◽  
C. Gomez-Manzano ◽  
W. K. Alfred Yung ◽  
A. P. Kyritsis
Keyword(s):  
Tumor Suppressor ◽  
Tumor Suppressor Genes ◽  
Functional Role ◽  
Therapeutic Strategies ◽  
Suppressor Genes

scholarly journals The role of XPC protein deficiency in tobacco smoke-induced DNA hypermethylation of tumor suppressor genes

2013 ◽  
Vol 03 (04) ◽  
pp. 285-293 ◽  
Author(s):  
Gan Wang ◽  
Le Wang ◽  
Vanitha Bhoopalan ◽  
Yue Xi ◽  
Deepak K. Bhalla ◽  
...  
Keyword(s):  
Tumor Suppressor ◽  
Tobacco Smoke ◽  
Tumor Suppressor Genes ◽  
Protein Deficiency ◽  
Dna Hypermethylation ◽  
Suppressor Genes

scholarly journals Loss of Heterozygosity at the Ink4a/ArfLocus Facilitates Abelson Virus Transformation of Pre-B Cells

2000 ◽  
Vol 74 (20) ◽  
pp. 9479-9487 ◽  
Author(s):  
Justin Mostecki ◽  
Anne Halgren ◽  
Arash Radfar ◽  
Zohar Sachs ◽  
James Ravitz ◽  
...  
Keyword(s):  
B Cells ◽  
Tumor Suppressor ◽  
Loss Of Heterozygosity ◽  
Cell Lines ◽  
Tumor Suppressor Genes ◽  
Single Copy ◽  
Transformation Process ◽  
Suppressor Genes ◽  
Abelson Virus

ABSTRACT In many tumor systems, analysis of cells for loss of heterozygosity (LOH) has helped to clarify the role of tumor suppressor genes in oncogenesis. Two important tumor suppressor genes, p53 and the Ink4a/Arf locus, play central roles in the multistep process of Abelson murine leukemia virus (Ab-MLV) transformation. p53 and the p53 regulatory protein, p19Arf, are required for the apoptotic crisis that characterizes the progression of primary transformed pre-B cells to fully malignant cell lines. To search for other tumor suppressor genes which may be involved in the Ab-MLV transformation process, we used endogenous proviral markers and simple-sequence length polymorphism analysis to screen Abelson virus-transformed pre-B cells for evidence of LOH. Our survey reinforces the role of the p53-p19 regulatory pathway in transformation; 6 of 58 cell lines tested had lost sequences on mouse chromosome 4, including theInk4a/Arf locus. Consistent with this pattern, a high frequency of primary pre-B-cell transformants derived fromInk4a/Arf +/− mice became established cell lines. In addition, half of them retained the single copy of the locus when the transformation process was complete. These data demonstrate that a single copy of the Ink4a/Arf locus is not sufficient to fully mediate the effects of these genes on transformation.

scholarly journals Decitabine-Induced Changes in Human Myelodysplastic Syndrome Cell Line SKM-1 Are Mediated by FOXO3A Activation

2017 ◽  
Vol 2017 ◽  
pp. 1-12 ◽  
Author(s):  
Wen Zeng ◽  
Hanjun Dai ◽  
Ming Yan ◽  
Xiaojun Cai ◽  
Hong Luo ◽  
...  
Keyword(s):  
Tumor Suppressor ◽  
Cell Line ◽  
Tumor Suppressor Genes ◽  
Therapeutic Effects ◽  
Suppressor Genes ◽  
Recommended Treatment ◽  
Cycle Arrest ◽  
Induced Changes ◽  
Hyperphosphorylated Form

The epigenetic silencing of tumor suppressor genes in myelodysplastic syndromes (MDS) can potentially confer a growth advantage to individual cellular clones. Currently, the recommended treatment for patients with high-risk MDS is the methylation agent decitabine (DAC), a drug that can induce the reexpression of silenced tumor suppressor genes. We investigated the effects of DAC treatment on the myeloid MDS cell line SKM-1 and investigated the role of FOXO3A, a potentially tumor-suppressive transcription factor, by silencing its expression prior to DAC treatment. We found that FOXO3A exists in an inactive, hyperphosphorylated form in SKM-1 cells, but that DAC both induces FOXO3A expression and reactivates the protein by reducing its phosphorylation level. Furthermore, we show that this FOXO3A activation is responsible for the DAC-induced differentiation of SKM-1 cells into monocytes, as well as for SKM-1 cell cycle arrest, apoptosis, and autophagy. Collectively, these results suggest that FOXO3A reactivation may contribute to the therapeutic effects of DAC in MDS.

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