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. Author manuscript; available in PMC: 2020 Mar 26.
Published in final edited form as: Biol Trace Elem Res. 2015 Mar 22;166(1):34–40. doi: 10.1007/s12011-015-0306-7

Fig. 2.

Fig. 2

Arsenic impact on mitotic progression. Progression from prophase through telophase to aneuploid progeny is diagrammed across the middle of the figure. Key events in the transitions are driven by cyclin B/CDK1 activity (prophase to metaphase progression) or inactivation (mitotic exit: metaphase to anaphase transition) and by separase activation and cleavage of cohesins to allow chromatid separation in anaphase. Cyclin B and securin are ubiquitinylated by the anaphase promoting complex/cyclosome (APC/C) and degraded by the proteasome. Cyclin B and securin are stabilized by arsenic (As) exposure. Arsenic induces p53 expression which, in turn, induces CDKN1A that then inhibits CDK1 activity and allows mitotic exit. miR-186 is overexpressed in arsenic-induced aquamous cell carcinoma and is known to suppress securin expression. It is hypothesized that the lower levels of securin would allow separase activation in the presence of arsenic and also would contribute to aneuploidy by inducing premature chromatid separation