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Loss of UGT1A potentiates ER stress induced by actinomycin D, etoposide, or DSS treatment. LS180 and HT29 cells were pretreated with UGT1A siRNA or nonspecific siRNA for 48 hours and then incubated with actinomycin D (ActD, 40 nM) or etoposide (Eto, 80 μM) for 36 hours. Ugt1ΔIEC and Ugt1F/F mice were treated with 3% DSS in drinking water and colon tissues were collected. Expression of ER stress-responsive genes was quantitated by Q-PCR.
