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To provide mechanistic insights into the effect of miR-221 on apoptosis, we measured the levels of apoptosis-associated proteins. Treatment with etoposide was associated with a marked decrease in the levels of Bcl-2, Bcl-XL, and Mcl-1 in etoposide-sensitive cells. In contrast, in etoposide-resistant cells the levels of antiapoptotic proteins were unaffected by the treatment ([Figure [4](#fig4){ref-type=”fig”}](#fig4){ref-type=”fig”}A). Next, we studied the effect of the miR-221 mimic and inhibitor on the levels of apoptotic proteins. The results indicated that the overexpression or the inhibition of miR-221 did not affect the levels of Bcl-2, Bcl-XL, or Mcl-1 in both etoposide-sensitive and -resistant cells. This suggests that etoposide treatment induces apoptosis by a mechanism independent of Bcl-2, Bcl-XL, and Mcl-1 ([Figure [4](#fig4){ref-type=”fig”}](#fig4){ref-type=”fig”}B). We further studied the effect of miR-221 on the levels of mitogen-activated protein kinase (MAPK) and Janus kinase (JAK)/signal transducer and activator of transcription (STAT) signaling, the major pathways involved in cell survival and apoptosis. The results indicated that etoposide treatment did not alter the levels of JAK1, JAK2, or STAT1 and 2 ([Figure S1](
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