Role of tumor suppressor genes in determining radiation-induced G1 arrest and transformation in human cells

1995 ◽  
Vol 3 (6) ◽  
pp. 268-271
Author(s):  
Chuan-Yuan Li ◽  
Hatsumi Nagasawa ◽  
John B. Little
Neurology ◽  
1998 ◽  
Vol 51 (5) ◽  
pp. 1250-1255 ◽  
Author(s):  
J. Fueyo ◽  
C. Gomez-Manzano ◽  
W. K. Alfred Yung ◽  
A. P. Kyritsis

2013 ◽  
Vol 03 (04) ◽  
pp. 285-293 ◽  
Author(s):  
Gan Wang ◽  
Le Wang ◽  
Vanitha Bhoopalan ◽  
Yue Xi ◽  
Deepak K. Bhalla ◽  
...  

2000 ◽  
Vol 74 (20) ◽  
pp. 9479-9487 ◽  
Author(s):  
Justin Mostecki ◽  
Anne Halgren ◽  
Arash Radfar ◽  
Zohar Sachs ◽  
James Ravitz ◽  
...  

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.


2017 ◽  
Vol 2017 ◽  
pp. 1-12 ◽  
Author(s):  
Wen Zeng ◽  
Hanjun Dai ◽  
Ming Yan ◽  
Xiaojun Cai ◽  
Hong Luo ◽  
...  

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.


MicroRNA ◽  
2020 ◽  
Vol 9 (2) ◽  
pp. 82-92 ◽  
Author(s):  
Fasoulakis Zacharias ◽  
Daskalakis George ◽  
Diakosavvas Michail ◽  
Papapanagiotou Ioannis ◽  
Theodora Marianna ◽  
...  

Aim:: To provide a review considering microRNAs regulating oncogenes and tumor suppressor genes during the different stages of cell cycle, controlling carcinogenesis. Methods:: The role of microRNAs involved as oncogenes’ and tumor suppressor genes’ regulators in cancer was searched in the relevant available literature in MEDLINE, including terms such as “microRNA”, “oncogenes”, “tumor suppressor genes”, “metastasis”, “cancer” and others. Results:: MicroRNAs determine the expression levels of multiple cell cycle regulators, such as cyclins, cyclin dependent kinases and other major cell cycle activators including retinoblastoma 1 (RB- 1) and p53, resulting in alteration and promotion/inhibition of the cell cycle. Conclusion:: MicroRNAs are proven to have a key role in cancer pathophysiology by altering the expression profile of different regulator proteins during cell division cycle and DNA replication. Thus, by acting as oncogenes and tumor suppressor genes, they can either promote or inhibit cancer development and formation, revealing their innovative role as biomarkers and therapeutic tools.


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