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Biometals. 2018 Aug;31(4):477-487. doi: 10.1007/s10534-018-0093-7. Epub 2018 Mar 16.

Hexavalent chromium, a lung carcinogen, confers resistance to thermal stress and interferes with heat shock protein expression in human bronchial epithelial cells.

Author information

1
Molecular Physical Chemistry Research Unit and Department of Life Sciences, University of Coimbra, Calçada Martim de Freitas, 3000-456, Coimbra, Portugal.
2
Instituto de Medicina Molecular, Faculty of Medicine, University of Lisbon, Lisbon, Portugal.
3
CNC - Center for Neuroscience and Cell Biology, University of Coimbra, UC Biotech Building, Lot 8A, Biocant Park, 3060-197, Cantanhede, Portugal.
4
Molecular Physical Chemistry Research Unit and Department of Life Sciences, University of Coimbra, Calçada Martim de Freitas, 3000-456, Coimbra, Portugal. leonardo.ferreira@ucsf.edu.
5
Department of Molecular and Cellular Biology, Harvard University, Cambridge, MA, USA. leonardo.ferreira@ucsf.edu.
6
Department of Surgery and Diabetes Center, University of California, San Francisco, 513 Parnassus Avenue, HSE-520, San Francisco, CA, 94143, USA. leonardo.ferreira@ucsf.edu.
7
Molecular Physical Chemistry Research Unit and Department of Life Sciences, University of Coimbra, Calçada Martim de Freitas, 3000-456, Coimbra, Portugal. amurbano@ci.uc.pt.
8
Centro de Investigação Em Meio Ambiente, Genética E Oncobiologia (CIMAGO), University of Coimbra, Coimbra, Portugal. amurbano@ci.uc.pt.

Abstract

Exposure to hexavalent chromium [Cr(VI)], a lung carcinogen, triggers several types of cellular stresses, namely oxidative, genotoxic and proteotoxic stresses. Given the evolutionary character of carcinogenesis, it is tempting to speculate that cells that survive the stresses produced by this carcinogen become more resistant to subsequent stresses, namely those encountered during neoplastic transformation. To test this hypothesis, we determined whether pre-incubation with Cr(VI) increased the resistance of human bronchial epithelial cells (BEAS-2B cells) to the antiproliferative action of acute thermal shock, used here as a model for stress. In line with the proposed hypothesis, it was observed that, at mildly cytotoxic concentrations, Cr(VI) attenuated the antiproliferative effects of both cold and heat shock. Mechanistically, Cr(VI) interfered with the expression of two components of the stress response pathway: heat shock proteins Hsp72 and Hsp90α. Specifically, Cr(VI) significantly depleted the mRNA levels of the former and the protein levels of the latter. Significantly, these two proteins are members of heat shock protein (Hsp) families (Hsp70 and Hsp90, respectively) that have been implicated in carcinogenesis. Thus, our results confirm and extend previous studies showing the capacity of Cr(VI) to interfere with the expression of stress response components.

KEYWORDS:

Heat shock proteins; Hexavalent chromium; Lung carcinogen; Stress response; Thermal shock

PMID:
29549560
DOI:
10.1007/s10534-018-0093-7

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