Mitochondrial transcription factor A regulated ionizing radiation-induced mitochondrial biogenesis in human lung adenocarcinoma A549 cells

Mitochondrial transcription factor A (TFAM), the first well-characterized transcription factor from vertebrate mitochondria, is closely related to mitochondrial DNA (mtDNA) maintenance and repair. Recent evidence has shown that the ratio of mtDNA to nuclearDNA (nDNA) is increased in both human cells...

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Published in:	Journal of radiation research Vol. 54; no. 6; pp. 998 - 1004
Main Authors:	Yu, Jing, Wang, Qisen, Chen, Ni, Sun, Yuxiang, Wang, Xiaofei, Wu, Lijun, Chen, Shaopeng, Yuan, Hang, Xu, An, Wang, Jun
Format:	Journal Article
Language:	English
Published:	England Oxford University Press 01-11-2013
Subjects:	Adenocarcinoma Adenocarcinoma - pathology Adenocarcinoma - physiopathology Biology Biosynthesis Cell Line, Tumor Cells (Biology) Cytochrome c Cytochrome oxidase Deoxyribonucleic acid DNA Copy Number Variations - genetics DNA, Mitochondrial - genetics DNA-Binding Proteins - metabolism Dose-Response Relationship, Radiation Electron Transport Complex IV - metabolism Human Humans Ionizing radiation Lungs Maintenance Mitochondria Mitochondrial DNA Mitochondrial Proteins - metabolism Mitochondrial Turnover - radiation effects Oxidase Radiation Dosage RNA Transcription Factors - metabolism Up-Regulation - radiation effects Vertebrates mitochondrial transcription factor A mitochondrial biogenesis mitochondrial DNA ionizing radiation
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Abstract	Mitochondrial transcription factor A (TFAM), the first well-characterized transcription factor from vertebrate mitochondria, is closely related to mitochondrial DNA (mtDNA) maintenance and repair. Recent evidence has shown that the ratio of mtDNA to nuclearDNA (nDNA) is increased in both human cells and murine tissues after ionizing radiation (IR). However, the underlying mechanism has not as yet been clearly identified. In the present study, we demonstrated that in human lung adenocarcinoma A549 cells, expression of TFAM was upregulated, together with the increase of the relative mtDNA copy number and cytochrome c oxidase (COX) activity after -particle irradiation. Furthermore, short hairpin RNA (shRNA)-mediated TFAM knockdown inhibited the enhancement of the relative mtDNA copy number and COX activity caused by -particles. Taken together, our data suggested that TFAM plays a crucial role in regulating mtDNA amplification and mitochondrial biogenesis under IR conditions.
AbstractList	Mitochondrial transcription factor A (TFAM), the first well-characterized transcription factor from vertebrate mitochondria, is closely related to mitochondrial DNA (mtDNA) maintenance and repair. Recent evidence has shown that the ratio of mtDNA to nuclearDNA (nDNA) is increased in both human cells and murine tissues after ionizing radiation (IR). However, the underlying mechanism has not as yet been clearly identified. In the present study, we demonstrated that in human lung adenocarcinoma A549 cells, expression of TFAM was upregulated, together with the increase of the relative mtDNA copy number and cytochrome c oxidase (COX) activity after α-particle irradiation. Furthermore, short hairpin RNA (shRNA)-mediated TFAM knockdown inhibited the enhancement of the relative mtDNA copy number and COX activity caused by α-particles. Taken together, our data suggested that TFAM plays a crucial role in regulating mtDNA amplification and mitochondrial biogenesis under IR conditions. Mitochondrial transcription factor A (TFAM), the first well-characterized transcription factor from vertebrate mitochondria, is closely related to mitochondrial DNA (mtDNA) maintenance and repair. Recent evidence has shown that the ratio of mtDNA to nuclearDNA (nDNA) is increased in both human cells and murine tissues after ionizing radiation (IR). However, the underlying mechanism has not as yet been clearly identified. In the present study, we demonstrated that in human lung adenocarcinoma A549 cells, expression of TFAM was upregulated, together with the increase of the relative mtDNA copy number and cytochrome c oxidase (COX) activity after alpha -particle irradiation. Furthermore, short hairpin RNA (shRNA)-mediated TFAM knockdown inhibited the enhancement of the relative mtDNA copy number and COX activity caused by alpha -particles. Taken together, our data suggested that TFAM plays a crucial role in regulating mtDNA amplification and mitochondrial biogenesis under IR conditions. Mitochondrial transcription factor A (TFAM), the first well-characterized transcription factor from vertebrate mitochondria, is closely related to mitochondrial DNA (mtDNA) maintenance and repair. Recent evidence has shown that the ratio of mtDNA to nuclearDNA (nDNA) is increased in both human cells and murine tissues after ionizing radiation (IR). However, the underlying mechanism has not as yet been clearly identified. In the present study, we demonstrated that in human lung adenocarcinoma A549 cells, expression of TFAM was upregulated, together with the increase of the relative mtDNA copy number and cytochrome c oxidase (COX) activity after [alpha]-particle irradiation. Furthermore, short hairpin RNA (shRNA)-mediated TFAM knockdown inhibited the enhancement of the relative mtDNA copy number and COX activity caused by [alpha]-particles. Taken together, our data suggested that TFAM plays a crucial role in regulating mtDNA amplification and mitochondrial biogenesis under IR conditions. Keywords: mitochondrial transcription factor A, ionizing radiation, mitochondrial DNA, mitochondrial biogenesis Mitochondrial transcription factor A (TFAM), the first well-characterized transcription factor from vertebrate mitochondria, is closely related to mitochondrial DNA (mtDNA) maintenance and repair. Recent evidence has shown that the ratio of mtDNA to nuclearDNA (nDNA) is increased in both human cells and murine tissues after ionizing radiation (IR). However, the underlying mechanism has not as yet been clearly identified. In the present study, we demonstrated that in human lung adenocarcinoma A549 cells, expression of TFAM was upregulated, together with the increase of the relative mtDNA copy number and cytochrome c oxidase (COX) activity after -particle irradiation. Furthermore, short hairpin RNA (shRNA)-mediated TFAM knockdown inhibited the enhancement of the relative mtDNA copy number and COX activity caused by -particles. Taken together, our data suggested that TFAM plays a crucial role in regulating mtDNA amplification and mitochondrial biogenesis under IR conditions.
Audience	Academic
Author	Xu, An Yu, Jing Yuan, Hang Wang, Xiaofei Wang, Qisen Wu, Lijun Chen, Shaopeng Wang, Jun Sun, Yuxiang Chen, Ni
AuthorAffiliation	1 School of Nuclear Science and Technology, University of Science and Technology of China, Hefei 230027, PR China 2 Key Laboratory of Ion Beam Bioengineering, Chinese Academy of Sciences, Shushan Road No. 350, Hefei 230031, PR China
AuthorAffiliation_xml	– name: 2 Key Laboratory of Ion Beam Bioengineering, Chinese Academy of Sciences, Shushan Road No. 350, Hefei 230031, PR China – name: 1 School of Nuclear Science and Technology, University of Science and Technology of China, Hefei 230027, PR China
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SubjectTerms	Adenocarcinoma Adenocarcinoma - pathology Adenocarcinoma - physiopathology Biology Biosynthesis Cell Line, Tumor Cells (Biology) Cytochrome c Cytochrome oxidase Deoxyribonucleic acid DNA Copy Number Variations - genetics DNA, Mitochondrial - genetics DNA-Binding Proteins - metabolism Dose-Response Relationship, Radiation Electron Transport Complex IV - metabolism Human Humans Ionizing radiation Lungs Maintenance Mitochondria Mitochondrial DNA Mitochondrial Proteins - metabolism Mitochondrial Turnover - radiation effects Oxidase Radiation Dosage RNA Transcription Factors - metabolism Up-Regulation - radiation effects Vertebrates
Title	Mitochondrial transcription factor A regulated ionizing radiation-induced mitochondrial biogenesis in human lung adenocarcinoma A549 cells
URI	https://www.ncbi.nlm.nih.gov/pubmed/23645454 https://search.proquest.com/docview/1458185159 https://search.proquest.com/docview/1732811040 https://search.proquest.com/docview/1786197795 https://pubmed.ncbi.nlm.nih.gov/PMC3823773
Volume	54
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