Journal
BIOMETALS
Volume 31, Issue 4, Pages 477-487Publisher
SPRINGER
DOI: 10.1007/s10534-018-0093-7
Keywords
Hexavalent chromium; Lung carcinogen; Thermal shock; Stress response; Heat shock proteins
Categories
Funding
- Centro de Investigacao em Meio Ambiente, Genetica e Oncobiologia (CIMAGO), Portugal [16/12]
- Fundacao para a Ciencia e a Tecnologia (FCT), Portugal [UID/MULTI/00070/2013, SFRH/BPD/101169/2014, BII/FCTUC/C2008/QFM/BQ/2aFASE]
- Fundação para a Ciência e a Tecnologia [UID/Multi/00070/2013] Funding Source: FCT
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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 Hsp90 alpha. 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.
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