Correlation among loss of heterozygosity, promoter methylation and protein expression of MLH1 in larynx cancer

Author(s):  
Robert Smigiel ◽  
Agnieszka Stembalska-Kozlowska ◽  
Farhad Mirghomizadeh ◽  
Tomasz Krecicki ◽  
Tomasz Zatonski ◽  
...  
2021 ◽  
Vol 20 ◽  
pp. 153303382098011
Author(s):  
Junjun Shu ◽  
Ling Xiao ◽  
Sanhua Yan ◽  
Boqun Fan ◽  
Xia Zou ◽  
...  

Objective: Ovarian cancer (OC) ranks one of the most prevalent fatal tumors of female genital organs. Aberrant promoter methylation triggers changes of microRNA (miR)-375 in OC. Our study aimed to evaluate the mechanism of methylated miR-375 promoter region in OC cell malignancy and to seek the possible treatment for OC. Methods: miR-375 promoter methylation level in OC tissues and cells was detected. miR-375 expression in OC tissues and cell lines was compared with that in demethylated cells. Role of miR-375 in OC progression was measured. Dual-luciferase reporter gene assay was utilized to verify the targeting relationship between miR-375 and Yes-associated protein 1 (YAP1). Then, Wnt/β-catenin pathway-related protein expression was tested. Moreover, xenograft transplantation was applied to confirm the in vitro experiments. Results: Highly methylated miR-375 was seen in OC tissues and cell lines, while its expression was decreased as the promoter methylation increased. Demethylation in OC cells brought miR-375 back to normal level, with obviously declined cell invasion, migration and viability and improved apoptosis. Additionally, miR-375 targeted YAP1 to regulate the Wnt/β-catenin pathway protein expression. Overexpressed YAP1 reversed the protein expression, promoted cell invasion, migration and viability while reduced cell apoptosis. Overexpressed miR-375 in vivo inhibited OC progression. Conclusion: Our study demonstrated that demethylated miR-375 inhibited OC growth by targeting YAP1 and downregulating the Wnt/β-catenin pathway. This investigation may offer novel insight for OC treatment.


2007 ◽  
Vol 134 (5) ◽  
pp. 579-589 ◽  
Author(s):  
Antal Csepregi ◽  
Christoph Röcken ◽  
Juliane Hoffmann ◽  
Ping Gu ◽  
Stephan Saliger ◽  
...  

2005 ◽  
Vol 206 (4) ◽  
pp. 409-416 ◽  
Author(s):  
S Pizzi ◽  
C Azzoni ◽  
L Bottarelli ◽  
N Campanini ◽  
T D'Adda ◽  
...  

2013 ◽  
Vol 3 ◽  
pp. 263-271
Author(s):  
Katarzyna Starska ◽  
Ewa Forma ◽  
Iwona Lewy-Trenda ◽  
Paweł Papież ◽  
Jan Woś ◽  
...  

2004 ◽  
Vol 101 (2) ◽  
pp. 574-579 ◽  
Author(s):  
N. A. C. S. Wong ◽  
M. P. Britton ◽  
G. S. Choi ◽  
T. K. Stanton ◽  
D. C. Bicknell ◽  
...  

Placenta ◽  
2014 ◽  
Vol 35 (10) ◽  
pp. A15-A16
Author(s):  
Yota Shimanuki ◽  
Hiroyuki Mitomi ◽  
Shintaro Makino ◽  
Atsuo Itakura ◽  
Satoru Takeda ◽  
...  

2011 ◽  
Vol 29 (2) ◽  
pp. 1292-1296 ◽  
Author(s):  
Kai Tang ◽  
Qiang Jin ◽  
Wei Yan ◽  
Wei Zhang ◽  
Gan You ◽  
...  

2020 ◽  
Vol 2020 ◽  
pp. 1-17 ◽  
Author(s):  
Xiu Hong Yang ◽  
Bao Long Zhang ◽  
Xiao Meng Zhang ◽  
Jin Dong Tong ◽  
Yan Hong Gu ◽  
...  

To explore whether epigallocatechin-3-gallate (EGCG) improves renal damage in diabetic db/db mice and high-glucose- (HG-) induced injury in HK-2 cells by regulating the level of Klotho gene promoter methylation. Western blotting was used to detect the protein expression levels of DNA methyltransferase 1 (DNMT1), DNMT3a, DNMT3b, transforming growth factor-β1 (TGF-β1), α-smooth muscle actin (α-SMA), and Klotho. The methylation level of the Klotho gene promoter was detected by pyrosequencing. Chromatin immunoprecipitation was used to detect the binding of the Klotho gene promoter to DNMT1 and DNMT3a. The expression of oxidative stress markers (reactive oxygen species (ROS), superoxide dismutase (SOD), malondialdehyde (MDA), catalase (CAT), and 8-hydroxy-2′-deoxyguanosine (8-OHdG)) and inflammatory cytokines (interleukin-1β (IL-1β), IL-6, and tumor necrosis factor-α (TNF-α)) in kidney homogenates was also measured using ELISA. Klotho and DNMT3b protein expression was upregulated, while DNMT1, DNMT3a, TGF-β1, and α-SMA protein expression was downregulated after EGCG treatment. EGCG treatment also reduced the methylation level of the Klotho gene promoter as well as the binding of DNMT3a to the Klotho gene promoter. In addition, EGCG treatment significantly decreased the levels of ROS, MDA, 8-OHdG, IL-1β, IL-6, and TNF-α and increased the levels of CAT and SOD. Under HG conditions, EGCG regulated Klotho gene promoter methylation via DNMT3a and decreased the methylation level of the Klotho gene promoter, thereby upregulating the expression of the Klotho protein to exert its protective effect.


2012 ◽  
Vol 31 (1) ◽  
pp. 15-24 ◽  
Author(s):  
Colleen L. Doçi ◽  
Tanmayi P. Mankame ◽  
Alexander Langerman ◽  
Kelly R. Ostler ◽  
Rajani Kanteti ◽  
...  

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