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. 2021 Aug 12;13(16):4052. doi: 10.3390/cancers13164052

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© 2021 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).

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Metal-induced ERK1/2 phosphorylation and proliferation. (a) Time course of ERK1/2 phosphorylation in thyrospheres exposed to metals at the concentration causing the greatest BrdU incorporation (see Table 1). The mean ± standard error of the mean of six separate experiments are shown. In all cases, the metal-induced increase was significant at 5 min, when it reached the peak value (except for Hg and W, which remained elevated for up to 15 min). (b) The effect of the ERK1/2 inhibitor PD98059 on ERK1/2 phosphorylation and on thyrosphere proliferation (BrdU incorporation) after cell exposure to the indicated metals. In all cases, the significant inhibition of ERK1/2 activation was associated with a significant inhibition of BrdU incorporation. The bars indicate the mean ± standard error of the mean of three separate experiments (* p < 0.05, ** p < 0.01, and *** p < 0.001). Represented data from ref. [56].