Cinnamic aldehyde induces apoptosis of breast cancer cells via STAT3/cMyc pathway

Abstract

Abstract Signal transducer and activator of transcription 3 (STAT3) is known to be activated in numerous cancer types, including more than 40% of breast cancers. STAT3 ’s downstream gene cMyc serves as an important target in cancer treatment. However, the clinical availability of small-molecule inhibitors that can target cMyc are lacking.Cinnamic aldehyde (CA) has been reported to inhibit the proliferation of a variety of cancer cells, including those in breast cancer; however, its molecular mechanism remains unclear. This study examined CA induction of apoptosis in breast cancer cells via STAT3/cMyc pathway. The corresponding findings demonstrated that CA significantly inhibited the proliferation and migration of MDA-MB-231 cells, MCF-7 cells, and 4T1 cells in both a time and concentration-dependent manner. CA was also shown to enhance the effect of cMyc inhibitor 10074-G5 and was observed to be better than 10074-G5 in the same concentration. CA also inhibited the proliferation and migration of breast cancer cells, which may be related to the induction of breast cancer cells’ mitochondral apoptosis through the down-regulation of apoptosis-related proteins via STAT3/cMyc pathway. Accordingly, this study suggests that CA may serve as a novel cMyc inhibitor in breast cancer cells and should be further studied.