ArticleThe American journal of pathology2011
Aberrant cell proliferation by enhanced mitochondrial biogenesis via mtTFA in arsenical skin cancers.
Article in The American journal of pathology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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37 citing papers in PubMed, 90 citations in OpenAlex.
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- The mitochondrial RNA polymerase POLRMT promotes skin squamous cell carcinoma cell growth.Cell death discovery · 2022Article
- TSLP regulates mitochondrial ROS-induced mitophagy via histone modification in human monocytes.Cell & bioscience · 2022Article
- Mitochondrial plasticity supports proliferative outgrowth and invasion of ovarian cancer spheroids during adhesion.Frontiers in oncology · 2022Article
- Arsenic leads to autophagy of keratinocytes by increasing aquaporin 3 expression.Scientific reports · 2021Article
- An N-ethyl-N-Nitrosourea Mutagenesis Screen in Mice Reveals a Mutation inAnimals : an open access journal from MDPI · 2021Article
- Acrylamide Induces Mitophagy and Alters Macrophage Phenotype via Reactive Oxygen Species Generation.International journal of molecular sciences · 2021Article
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- A Peripheral CB1R Antagonist Increases Lipolysis, Oxygen Consumption Rate, and Markers of Beiging in 3T3-L1 Adipocytes Similar to RIM, Suggesting that Central Effects Can Be Avoided.International journal of molecular sciences · 2020Article
- Mitochondrial HMG-Box Containing Proteins: From Biochemical Properties to the Roles in Human Diseases.Biomolecules · 2020Review
- Cytoprotective role of humanin in lens epithelial cell oxidative stress‑induced injury.Molecular medicine reports · 2020Article
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- Arsenite exposure suppresses adipogenesis, mitochondrial biogenesis and thermogenesis via autophagy inhibition in brown adipose tissue.Scientific reports · 2019Article
- Arsenic-Induced Carcinogenesis and Immune Dysregulation.International journal of environmental research and public health · 2019Review
- Lactic Acidosis Promotes Mitochondrial Biogenesis in Lung Adenocarcinoma Cells, Supporting Proliferation Under Normoxia or Survival Under Hypoxia.Frontiers in oncology · 2019Article
- Peroxisome Proliferator-Activated ReceptorPPAR research · 2018Review
- Transcriptomic analysis of mitochondrial TFAM depletion changing cell morphology and proliferation.Scientific reports · 2017Article
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Arsenic-induced Bowen's disease (As-BD), a cutaneous carcinoma in situ, is thought to arise from gene mutation and uncontrolled proliferation. However, how mitochondria regulate the arsenic-induced cell proliferation remains unclear. The aim of this study was to clarify whether arsenic interfered with mitochondrial biogenesis and function, leading to aberrant cell proliferation in As-BD. Skin biopsy samples from patients with As-BD and controls were stained for cytochrome c oxidase (Complex IV), measured for mitochondrial DNA (mtDNA) copy number and the expression levels of mitochondrial biogenesis-related genes, including peroxisome proliferator-activated receptor gamma coactivator-1α (PGC-1α), nuclear respiratory factor 1 (NRF-1), and mitochondrial transcription factor A (mtTFA). The results showed that expression of cytochrome c oxidase, mtTFA, NRF-1, and PGC-1α was increased in As-BD compared with in healthy subjects. Treatment of primary keratinocytes with arsenic at concentrations lower than 1.0 μmol/L induced cell proliferation, along with enhanced mitochondrial biogenesis. Furthermore, we observed that the mitochondrial oxygen consumption rate and intracellular ATP level were increased in arsenic-treated keratinocytes. Blocking of mitochondrial function by oligomycin A (Complex V inhibitor) or knockdown of mtTFA by RNA interference abrogated arsenic-induced cell proliferation without affecting cyclin D1 expression. We concluded that mtTFA up-regulation, augmented mitochondrial biogenesis, and enhanced mitochondrial functions may contribute to arsenic-induced cell proliferation. Targeting mitochondrial biogenesis may help treat arsenical cancers at the stage of cell proliferation.
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