Moreover, protein phosphorylation analysis indicated that both compounds induced hyperphosphorylation of JNK, and ERK1/2, along with hypophosphorylation of p38 kinases.<h4>Conclusions</h4>P3C.1 and P3C.2 emerged as promising anti-breast cancer agents with dual mechanisms of action involving microtubule disruption and altered kinase signaling, leading to induction of apoptosis. This evidence concerns the gene MAPK3 and breast carcinoma.