Mitochondrial defects in cancer
TL;DR: A brief summary of the current understanding of mitochondrial genetics and biology is provided, the mtDNA alterations reported in various types of cancer are reviewed, and some perspective is offered as to the emergence of mtDNA mutations, their functional consequences in cancer development, and therapeutic implications.
read more
Abstract: Mitochondria play important roles in cellular energy metabolism, free radical generation, and apoptosis. Defects in mitochondrial function have long been suspected to contribute to the development and progression of cancer. In this review article, we aim to provide a brief summary of our current understanding of mitochondrial genetics and biology, review the mtDNA alterations reported in various types of cancer, and offer some perspective as to the emergence of mtDNA mutations, their functional consequences in cancer development, and therapeutic implications.
read more
Chat with Paper
AI Agents for this Paper
Find similar papers on Google Scholar, PubMed and Arxiv
Write a critical review of this paper
Analyze citations of this paper to find unaddressed research gaps
Citations
Mechanisms Adopted by Cancer Cells to Escape Apoptosis–a Review
Sayequa Dandoti
TL;DR: Cancer cells evade apoptosis through various mechanisms, including gene alterations, post-translational modifications, metabolic and mitochondrial changes, immunity escape, epigenetics, and dormancy, rendering them resistant to therapies and highlighting the need for further research.
Detection of Mitochondrial DNA and Apoptosis in Esophageal Squamous Cell Carcinoma TE-13 Cells
LIU Zongwen,FENG Fuming,WANG Yali,YANG Jianping,PANG Xia,WANG Feng,GUO Fengling,ZHENG Guoxiang,YAN Junyu,ZHANG Gongyuan,CHEN Kuisheng +10 more
Abstract: Aim:To detect the mitochondrial DNA(mtDNA) and apoptosis in esophageal squamous cell carcinoma(ESCC) TE-13 cells.Methods:TE-13 cells were allocated into 2 groups:EB treatment group and control group.RT-PCR was used to detect the expression of mtDNA,and apoptosis in the cells was detected by flow cytometry at days 4,8 and 12.Results:The result of mtDNA expression in EB treatment group gradually decreased from(0.467±0.031),(0.197±0.015) to 0 at days 4,8 and 12,control group was(0.660±0.046),(0.673±0.031)and(0.653±0.021),and there were significant differences between the two groups(Fgroup=1 133.878,Ftime=109.058,Finteraction=104.597;P0.001).The results of flow cytometry revealed that cell apoptosis rates in EB treatment group were significantly higher than those of control group at days 4,8 and 12(Fgroup=2 773.035,Ftime=407.652,Finteraction=406.641;P0.001).Conclusion:The inhibition of mtDNA duplication may prompt the apoptosis of TE-13 cells.
Mitochondrial Control Region Variants Related to Breast Cancer
Jorge Hermilo Vega Avalos,Luis Enrique Hernandez,Laura Y Zuñiga,María Guadalupe Sánchez-Parada,A. E. González Santiago,Luis Miguel Román Pintos,Rolando Castañeda Arellano,Luis Daniel Hernández-Ortega,Arieh R Mercado-Sesma,Felipe de Jesús Orozco-Luna,Raúl C. Baptista-Rosas +10 more
TL;DR: In this article , the mtDNA sequences associated with breast cancer cases were identified, of which 86 were complete and 38 were partial sequences, of these 86 complete sequences, 52 belonged to patients with a confirmed diagnosis of breast cancer, and 34 sequences were obtained from healthy mammary tissue of the same patients used as controls.
Manganese superoxide dismutase regulation and cancer.
TL;DR: Current knowledge of the relationship between manganese superoxide dismutase levels and cancer is summarized with a focus on the mechanisms regulating MnSOD expression.
Mitochondrial DNA Mutations in Grade II and III Glioma Cell Lines Are Associated with Significant Mitochondrial Dysfunction and Higher Oxidative Stress
Bee Hong Soon,Nor Azian Abdul Murad,Sue-Mian Then,Sue-Mian Then,Azizi Abu Bakar,Farizal Fadzil,Jegan Thanabalan,Mohd Saffari Mohd Haspani,Charng Jeng Toh,Azmi Mohd Tamil,Roslan Harun,Wan Zurinah Wan Ngah,A. Rahman A. Jamal +12 more
TL;DR: These non-synonymous mtDNA sequence variations were predicted to be pathogenic and could possibly lead to protein dysfunction, leading to oxidative phosphorylation impairment, mitochondria dysfunction and could create a vicious cycle of oxidative stress.
References
Sequence and organization of the human mitochondrial genome
Stephen Anderson,Alan T. Bankier,Bart Barrell,M.H.L. de Bruijn,Alan Coulson,J. Drouin,J. Drouin,Ian C. Eperon,Donald P. Nierlich,Donald P. Nierlich,Bruce A. Roe,Bruce A. Roe,Frederick Sanger,P. H. Schreier,Andrew J.H. Smith,Rodger Staden,Ian G. Young,Ian G. Young +17 more
- 09 Apr 1981
TL;DR: The complete sequence of the 16,569-base pair human mitochondrial genome is presented and shows extreme economy in that the genes have none or only a few noncoding bases between them, and in many cases the termination codons are not coded in the DNA but are created post-transcriptionally by polyadenylation of the mRNAs.
9.1K
Induction of apoptotic program in cell-free extracts : requirement for datp and cytochrome c
TL;DR: Cells undergoing apoptosis in vivo showed increased release of cy tochrome c to their cytosol, suggesting that mitochondria may function in apoptosis by releasing cytochrome c.
5.4K
Molecular characterization of mitochondrial apoptosis-inducing factor
Santos A. Susin,Hans K. Lorenzo,Naoufal Zamzami,Isabel Marzo,Bryan E. Snow,Joan Mangion,Etienne Jacotot,Paola Costantini,Markus Loeffler,Nathanael Larochette,David R. Goodlett,Ruedi Aebersold,David P. Siderovski,Josef M. Penninger,Guido Kroemer +14 more
TL;DR: The identification and cloning of an apoptosis-inducing factor, AIF, which is sufficient to induce apoptosis of isolated nuclei is reported, indicating that AIF is a mitochondrial effector of apoptotic cell death.
4.3K