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. 2012 Aug 10;7(8):e42921. doi: 10.1371/journal.pone.0042921

Figure 8. Model describing doxorubicin induction of FILIP1L and apoptosis.

Figure 8

Our data suggests that doxorubicin treatment significantly activates FILIP1L expression and requires both OCT1 and ATM/ATR/p 53 activity for this expression. Ectopic expression of FILIP1L is sufficient for significant apoptosis induction. It is unclear how and if ATM/ATR and p 53 interact with Oct1, or if they function in via a parallel pathway to modulate FILIP1L expression. These findings suggest that FILIP1L expression may mediate doxorubicin induced apoptosis during chemotherapy and pose the hypothesis that cancers with down-regulated FILIP1L expression may display elevated doxorubicin resistance.