Benzophenone-2 (BP2) is used as a UV screen in many cosmetics of daily use, which regularly come in contact with the human skin. It is well known that BP2 is an endocrine-disrupting chemical (EDC) that disrupts the thyroid hormone axis via the inhibition of thyroid peroxidase. However, the molecular mechanism of BP2-induced cellular toxicity remains unclear. We undertook a genome-wide analysis of transcriptional responses of human thyroid follicular carcinoma FTC-238 cells to non-toxic doses of BP2 (1 and $50;{mu}M$). Whole human genome microarrays detected a total of 4,495 genes that exhibited altered expression after exposure to both non-toxic doses of BP2 compared with a vehicle control, DMSO. We found that 534 and 4,142 genes showed different expression levels following treatment with the low and high nontoxic doses of BP2, respectively. Thus, low doses of BP2 can induce various changes in gene expression. The BP2 responsive genes were involved in glycolysis, translation, apoptosis, cell proliferation, generation of precursor metabolites and energy, and microtubulebased processes. Commonly expressed genes by $1;{mu}M$ and $50;{mu}M$ of BP2 treatments were associated with glycolysis components, including GAPDH, ENO1, PGK1, TROVE2, LDHA, ALDOA, and PKM2. The downregulated GAPDH, and ENO1 are typical glycolytic transcripts in glycolysis. The disruption of glycolysis including nutrients-replete conditions influences on cell cycle arrest or apoptosis. The possible roles of the responsive genes and their related pathways in BP2-induced cellular responses are discussed. This study helps to understand how cells respond to BP2 exposure via transcriptional regulation.