Transcriptional silencing of the TMS1/ASC tumour suppressor gene by an epigenetic mechanism in hepatocellular carcinoma cells

2007 ◽  
Vol 212 (2) ◽  
pp. 134-142 ◽  
Author(s):  
C Zhang ◽  
H Li ◽  
G Zhou ◽  
Q Zhang ◽  
T Zhang ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Transcriptional Silencing ◽  
Suppressor Gene ◽  
Tumour Suppressor Gene ◽  
Carcinoma Cells ◽  
Tumour Suppressor ◽  
Epigenetic Mechanism ◽  
Hepatocellular Carcinoma Cells

Conserved epigenetic changes in sporadic and HIV-associated high-grade B-cell lymphomas

2007 ◽  
Vol 25 (18_suppl) ◽  
pp. 18540-18540
Author(s):  
T. Crook ◽  
P. Smith ◽  
N. Syed ◽  
J. Stebbing ◽  
B. Griffin ◽  
...  
Keyword(s):  
B Cell ◽  
Cell Lines ◽  
Transcriptional Silencing ◽  
B Cell Lymphoma ◽  
Suppressor Gene ◽  
Tumour Suppressor Gene ◽  
Tumour Suppressor ◽  
Aberrant Methylation ◽  
Epigenetic Changes ◽  
B Cell Lymphomas

18540 Background: Transcriptional silencing represents a major mechanism of tumour suppressor gene inactivation in human tumours, including lymphoma. Here, we have compared patterns of aberrant methylation in sporadic and HIV-associated B cell lymphomas. Methods: We used methylation reversal/ micro-array analysis to seek novel genes subject to methylation-dependent transcriptional silencing in B cell lymphoma cell lines and primary B cell lymphomas from immune competent and HIV positive patients. Results: We describe the identification from these studies of a number of genes previously unreported as human tumour suppressors that are subject to transcriptional silencing in B lymphomas. Analysis of a subset of these genes, together with a panel of previously identified transcriptionally-silenced genes in primary B lymphomas, both sporadic and HIV-associated, revealed that patterns of aberrant methylation were highly conserved between the two patient groups. In contrast, we found no epigenetic changes in any of the analysed genes in EBV-immortalised B lymphoblastoid cell lines. Conclusions: These studies show that a similar subset of genes is subject to methylation-dependent transcriptional silencing in B lymphomas in sporadic and HIV-associated cases, implying that the same tumour suppressor pathways are inactivated and arguing that, at least epigenetically, these disorders are very similar disease entities. No significant financial relationships to disclose.

scholarly journals miR-9-3p plays a tumour-suppressor role by targeting TAZ (WWTR1) in hepatocellular carcinoma cells

2015 ◽  
Vol 113 (2) ◽  
pp. 252-258 ◽  
Author(s):  
T Higashi ◽  
H Hayashi ◽  
T Ishimoto ◽  
H Takeyama ◽  
T Kaida ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Carcinoma Cells ◽  
Tumour Suppressor ◽  
Hepatocellular Carcinoma Cells

scholarly journals The level of caveolin-1 expression determines response to TGF-β as a tumour suppressor in hepatocellular carcinoma cells

2017 ◽  
Vol 8 (10) ◽  
pp. e3098-e3098 ◽  
Author(s):  
Joaquim Moreno-Càceres ◽  
Daniel Caballero-Díaz ◽  
Zeribe Chike Nwosu ◽  
Christoph Meyer ◽  
Judit López-Luque ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Carcinoma Cells ◽  
Tumour Suppressor ◽  
Hepatocellular Carcinoma Cells ◽  
Caveolin 1

Alterations of tumour suppressor gene PPP2R1B in hepatocellular carcinoma

2007 ◽  
Vol 253 (1) ◽  
pp. 138-143 ◽  
Author(s):  
Huei-Chi Chou ◽  
Chien-Hung Chen ◽  
Hsuan-Shu Lee ◽  
Cha-Ze Lee ◽  
Guan-Tarn Huang ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Suppressor Gene ◽  
Tumour Suppressor Gene ◽  
Tumour Suppressor

scholarly journals Silencing of Testin expression is a frequent event in spontaneous lymphomas from Trp53-mutant mice

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Robert J. Weeks ◽  
Jackie L. Ludgate ◽  
Gwenn Le Mée ◽  
Rubina Khanal ◽  
Sunali Mehta ◽  
...  
Keyword(s):  
Mouse Models ◽  
Promoter Methylation ◽  
Mutant Mouse ◽  
Transcriptional Silencing ◽  
Suppressor Gene ◽  
Tumour Suppressor Gene ◽  
Tumour Suppressor ◽  
Mutant Mice ◽  
Suppressor Activity ◽  
Frequent Event

Abstract The tumour suppressor gene, TES, is frequently methylated in many human tumours. Previously, we demonstrated that TES promoter methylation and transcriptional silencing was the most common molecular abnormality detected in childhood acute lymphoblastic leukaemia (ALL). Trp53-mutant mouse models predominantly develop B- and T-cell lymphomas, which are widely considered equivalent to childhood T and B ALL. In this study, we examined expression of Tes transcript and Testin protein in spontaneous tumours obtained from three Trp53-mutant mouse models. Using immunohistochemistry, we report that 47% of lymphomas lacked Testin protein compared to only 7% of non-lymphoid tumours. Further examination of the lymphomas from Trp53-null and Trp53-mΔpro homozygous mutant mice revealed that 63% and 69% respectively of the isolated lymphomas were Testin negative, which is similar to reported rates in childhood T-ALL. Surprisingly, lymphomas from Trp53-Δ122 mice were frequently Testin positive (> 60%), suggesting that the presence of the Trp53-Δ122 protein appeared to mitigate the requirement for Tes silencing in lymphomagenesis. Quantitative RT-PCR results confirmed that this lack of Testin protein was due to Tes transcriptional silencing, although bisulfite sequencing demonstrated that this was not due to promoter methylation. These results are consistent with the Testin protein having lymphoid tumour suppressor activity in both mice and humans.

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