scholarly journals Mitochondrial DNA copy number is regulated by DNA methylation and demethylation of POLGA in stem and cancer cells and their differentiated progeny

2015 ◽  
Vol 6 (2) ◽  
pp. e1664-e1664 ◽  
Author(s):  
W Lee ◽  
J Johnson ◽  
D J Gough ◽  
J Donoghue ◽  
G L M Cagnone ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Mitochondrial Dna ◽  
Cancer Cells ◽  
Copy Number ◽  
Dna Copy Number ◽  
Mitochondrial Dna Copy Number

scholarly journals Mitochondrial DNA methylation and copy number predict body composition in a young female population

2019 ◽  
Vol 17 (1) ◽  
Author(s):  
Laura Bordoni ◽  
Vanessa Smerilli ◽  
Cinzia Nasuti ◽  
Rosita Gabbianelli
Keyword(s):  
Dna Methylation ◽  
Body Composition ◽  
Mitochondrial Dna ◽  
Copy Number ◽  
Buccal Swab ◽  
Dna Copy Number ◽  
Female Population ◽  
Mitochondrial Dna Copy Number ◽  
Buccal Swabs ◽  
D Loop

Abstract Background Since both genomic and environmental factors are involved in obesity etiology, several studies about the influence of adiposity on both nuclear DNA and mitochondrial DNA methylation patterns have been carried out. Nevertheless, few evidences exploring the usage of buccal swab samples to study mitochondrial DNA epigenetics can be found in literature. Methods In this study, mitochondrial DNA from buccal swabs collected from a young Caucasian population (n = 69) have been used to examine potential correlation between mitochondrial DNA copy number and methylation with body composition (BMI, WHtR and bioimpedance measurements). Results A negative correlation between mitochondrial DNA copy number and BMI was measured in females (p = 0.028), but not in males. The mean percentage of D-loop methylation is significantly higher in overweight than in lean female subjects (p = 0.003), and a specific CpG located in the D-loop shows per se an association with impaired body composition (p = 0.004). Body composition impairment is predicted by a combined variable including mtDNA copy number and the D-loop methylation (AUC = 0.785; p = 0.009). Conclusions This study corroborates the hypothesis that mitochondrial DNA carries relevant information about body composition. However, wider investigations able to validate the usage of mtDNA methylation from buccal swabs as a biomarker are warranted.

scholarly journals Abiraterone and MDV3100 inhibits the proliferation and promotes the apoptosis of prostate cancer cells through mitophagy

2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Jingli Han ◽  
Junhua Zhang ◽  
Wei Zhang ◽  
Dalei Zhang ◽  
Ying Li ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Mitochondrial Dna ◽  
Cancer Cells ◽  
Copy Number ◽  
Expression Level ◽  
Lncap Cells ◽  
Prostate Cancer Cells ◽  
Dna Copy Number ◽  
Treatment Groups ◽  
Mitochondrial Dna Copy Number

Abstract Background Abiraterone and MDV3100 are two effective anticancer agents for prostate cancer, however, the mechanism of their downstream action remains undefined. Methods A dual fluorescent biosensor plasmid was transfected in LNCaP cells to measure mitophagy. The DNA of LNCaP cells was extracted and performed with quantitative real-time PCR to detect mitochondrial DNA copy number. JC-1 staining was utilized to detect the mitochondrial membrane potential and electron microscope was performed to analyze mitochondrial morphology. Moreover, the protein levels of mitochondrial markers and apoptotic markers were detected by western blot. At last, the proliferation and apoptosis of LNCaP cells were analyzed with CCK-8 assay and flow cytometry after abiraterone or MDV3100 treatment. Results Mitophagy was induced by abiraterone and MDV3100 in LNCaP cells. The low expression level of mitochondrial DNA copy number and mitochondrial depolarization were further identified in the abiraterone or MDV3100 treatment groups compared with the control group. Besides, severe mitochondria swelling and substantial autophagy-lysosomes were observed in abiraterone- and MDV3100-treated LNCaP cells. The expression of mitochondria-related proteins, frataxin, ACO2 and Tom20 were significantly downregulated in abiraterone and MDV3100 treated LNCaP cells, whereas the expression level of inner membrane protein of mitochondria (Tim23) was significantly upregulated in the same condition. Moreover, the proliferation of LNCaP cells were drastically inhibited, and the apoptosis of LNCaP cells was increased in abiraterone or MDV3100 treatment groups. Meanwhile, the addition of mitophagy inhibitor Mdivi-1 (mitochondrial division inhibitor 1) could conversely elevate proliferation and constrain apoptosis of LNCaP cells. Conclusions Our results prove that both abiraterone and MDV3100 inhibit the proliferation, promote the apoptosis of prostate cancer cells through regulating mitophagy. The promotion of mitophagy might enhance the efficacy of abiraterone and MDV3100, which could be a potential strategy to improve chemotherapy with these two reagents.

scholarly journals Association of DNA Methylation and Mitochondrial DNA Copy Number with Human Semen Quality1

2014 ◽  
Vol 91 (4) ◽  
Author(s):  
Meiping Tian ◽  
Huaqiong Bao ◽  
Francis L. Martin ◽  
Jie Zhang ◽  
Liangpo Liu ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Mitochondrial Dna ◽  
Copy Number ◽  
Human Semen ◽  
Dna Copy Number ◽  
Mitochondrial Dna Copy Number
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