Cytotoxicity of sodium selenite in HaCaT cells induces cell death and alters the mRNA expression of PUMA,ATR, and mTOR genes |
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| Affiliation: | 1. School of Public Health, The Key Laboratory of Environmental Pollution Monitoring and Disease Control, Ministry of Education, Guizhou Medical University, Guiyang, 550025, China;2. Guizhou Orthopedics Hospital, Guiyang, 550007, China;1. Clinical Medical College, Dali University, Dali, Yunnan, China;2. Affiliated Hospital of Guizhou Medical University, Guiyang, China;3. Department of Oncology, Chongqing Hospital of Traditional Chinese Medicine, Chongqing, China;4. Xinqiao Hospital, Third Military Medical University (Army Medical University), Chongqing, China;1. School of Medicine, Universidad Panamericana, Mexico City, Mexico;2. Univerisidad de Papaloapan, Oaxaca, Mexico;3. Laboratory of Developmental Biology Research and Experimental Teratogenicity. Children’s Hospital of Mexico Federico Gomez (HIMFG), Mexico City, Mexico;1. Biotechnology Center, Cukurova University, Adana, Turkey;2. Vocational School of Imamoğlu, Cukurova University, Adana, Turkey;1. Center for Basic Medical Research & Department of Cardiovascular Surgery, TEDA International Cardiovascular Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Tianjin, China;2. Unit of Perfusion, Department of Cardiovascular Surgery, TEDA International Cardiovascular Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Tianjin, China;3. Department of Cardiovascular Surgery, The First Affiliated Hospital, Zhejiang University, Hangzhou, China;4. School of Pharmacy, Wannan Medical College, Wuhu, China;5. Department of Surgery, Oregon Health and Science University, Portland, Oregon, USA |
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| Abstract: | BackgroundBy identifying the molecular mechanisms underlying sodium selenite (Na2SeO3) cytotoxicity during exposure in non-tumor cells (HaCaT cells), we will improve the current understanding of its antiproliferative effects and modulation of gene expression in the main pathways related to the cell cycle, cell death, oxidative stress, and DNA damage and repair.MethodsNon-tumor HaCaT cells were treated with Na2SeO3 to induce cytotoxicity, and the effects were investigated using an MTT assay (cell viability), real-time cell analysis (profiling the cell index), flow cytometry (membrane integrity, cell cycle disruption, and apoptosis), a comet assay (genotoxicity, i.e., DNA damage), and RT-qPCR (mRNA expression of genes).ResultsTreatment with Na2SeO3 was cytotoxic at 10 μM, producing morphological changes in cells (cytoplasmic granulations); however, it did not have a genotoxic effect. Na2SeO3 induced cell membrane damage, cell death, and cell cycle arrest in HaCaT cells. It also altered the mRNA expression levels of PUMA, ATR, and mTOR genes. However, it had no effect on the mRNA expression of caspases or PARP1, BIRC5, BECN1, and c-MYC genes, suggesting that Na2SeO3 causes PUMA-dependent apoptosis in HaCaT cells. The mRNA expression of specific genes related to oxidative stress, DNA damage and repair, and cell cycle control were unchanged by Na2SeO3.ConclusionsWe demonstrated the cytotoxic effect of Na2SeO3 in HaCaT cells by analyzing mRNA expression patterns, changes in cell morphology, and proliferation kinetics. |
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| Keywords: | Cytotoxicity Antiproliferation Mechanism of action HaCaT |
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