Fig. 2

The illustration of the possible signaling circuits involved in MT1-MMP-mediated autophagy and apoptosis following ConA treatment. In the unfunctional-p53 tumor cells, ConA can induce P73, which leads to the translocation of FOXO transcription factors to the nucleus so that they can induce an apoptotic gene profile. Also, ConA can induce JAK/STAT-3, MAPK, and NF-κB signaling pathways, which all would carry on the autophagy and apoptosis processes by modulating some essential factors like inducing BNIP3 to exit from the nucleus and initiate both programmed cell death I and II. Moreover, via inhibiting the Akt signaling pathway, ConA can increase the cytoplasmic level of Ca²⁺, which results in the accumulation of unmatured MT1-MMP in the cytoplasm of cancer cells. In P53-containing cells, nevertheless, ConA activates p53 in a post-translational way to create a transient cell-cycle arrest, which will induce cellular DNA repair