Journal of Cancer Prevention : pISSN 2288-3649 / eISSN 2288-3657

Fig. 1.

Download original image
Fig. 1. The substrates of PIM (proviral integration site for moloney murine leukemia virus) kinase. PIM activates genes transcription and cell cycles, and inhibits apoptosis of cells by directly or indirectly regulation of targets. PIM directly phophorylates myelocytomatosis (MYC) (Ser62/Ser329), cell division cycle 25A (CDC25A), and Notch homolog 1, translocation-associated (Notch1) (Ser2152) for triggering transcriptional activation and cell cycles to promoting cancer cell proliferation. Phosphorylation by PIM also inactivates p21Cip1/Waf1 (Thr145)/p27Kip1 (Thr157) and BCL-2-associated agonist of cell death (BAD) (Ser112) for prohibiting cell cycle regulation and apoptosis. PIM possibly phosphorylates C-X-C chemokine recepter type 4 (CXCR4) thereby enhances chronic lymphocytic leukemia cell survival, and decreases reactive oxygen species (ROS) by regulation of Nrf2 in the hypoxic tumor cells.
Journal of Cancer Prevention 2018;23:109-16
© 2018 Journal of Cancer Prevention