Journal
CHEMOSPHERE
Volume 266, Issue -, Pages -Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.chemosphere.2020.128994
Keywords
PM10; NORAD; A549; Mitotic slippage; Chromosomal segregation; Aneuploidy
Categories
Funding
- Consejo Nacional de Ciencia y Tecnologia, Mexico [SEP-CONACYTCB-2011-180471, SEP-CONACYTCB-2015-01-255150]
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PM10 exposure increases chromosomal instability in lung cancer cells by affecting the expression levels of long non-coding RNA NORAD and components of the spindle assembly checkpoint (SAC). Aneuploidy events are induced by SAC deregulation due to PM10 treatment.
Air pollution is a worldwide problem that affects human health predominantly in the largest cities. Particulate matter of 10 mm or less in diameter (PM10) is considered a risk factor for multiple diseases, including lung cancer. The long non-coding RNA NORAD and the components of the spindle assembly checkpoint (SAC) ensure proper chromosomal segregation. Alterations in the SAC cause aneuploidy, a feature associated with carcinogenesis. In this study, we demonstrated that PM10 treatment increased the expression levels of NORAD as well as those of SAC components mitotic arrest deficient 1 (MAD1L1), mitotic arrest deficient 2 (MAD2L1), BubR1 (BUB1B), aurora B (AURKB), and survivin (BIRC5) in the lung A549 cell line. We also demonstrated that MAD1L1, MAD2L1, and BUB1B expression levels were reduced when cells were transfected with small interfering RNAs (siRNAs) against NORAD. Interestingly, the expression levels of AURKB and BIRC5 (survivin) were not affected by transfection with NORAD siRNAs. Cells treated with PM10 exhibited a decrease in mitotic arrest and an increase in micronuclei frequency in synchronized A549 cells. PM10 exposure induced aneuploidy events as a result of SAC deregulation. We also observed a reduction in the protein levels of Pumilio 1 after PM10 treatment. Our results provide novel clues regarding the effect of PM10 in the generation of chromosomal instability, a phenotype observed in lung cancer cells. (C) 2020 Elsevier Ltd. All rights reserved.
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