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Roles of ROS, Akt, ERK signaling in arsenic‐induced cell transformation and tumor growth

Arsenic is strongly associated with lung cancer. But mechanism of arsenic in carcinogenesis still remains to be elucidated. This study sets to understand roles of reactive oxygen species (ROS) and signaling molecules in arsenic‐inducing cell transformation and tumor growth using lung bronchial epithelial (BEAS‐2B) cells. Acute arsenic treatment and arsenic‐transformed (As‐T) cells have much higher ROS generation. Arsenic activated Akt and ERK signaling which was abated with ROS inhibition via catalase treatment. As‐T cells increased cell proliferation and colony formation in soft agar. Interruption of ROS generation, PI3K/Akt, and MEK/ERK signaling significantly decreased proliferation and colony formation in As‐T cells. As‐T cells formed a greater number of primary tumors with larger tumor volume in immune‐deficient mice when compared to untreated control cells. Tumor weight was significantly reduced with catalase treatment. Tumor formation of As‐T cells was completely ablated with Akt interruption. We conclude that arsenic‐induced cell transformation and tumor growth requires ROS generation and Akt/ERK signaling. Funding was provided by National Institutes of Health and American Cancer Society.