Fig. 4

Signaling pathways and genes controlling PLAC8 expression and its regulatory system. PLAC8 regulation is driven by different factors in both the nucleus and cytoplasm. It is important to point out that published mechanisms of PLAC8 regulation are not yet completely understood. Studies have shown that growth-related signaling pathways, such as the AKT, MAPK and TGF-β/Smad pathways, interact with PLAC8. Some drugs, such as curcumin and PAM, directly and indirectly affect PLAC8 levels. In addition, PLAC8, as a transcription factor, promotes C/EBPβ transcription and inhibits PU.1 transcription. The dashed lines depict mechanisms that are not completely understood. C/EBPβ, enhancer-binding protein β; ALDH1A1, aldehyde dehydrogenase 1 family member A1; CDC42, cell division control protein 42; POU5F1, POU Class 5 homeobox 1; RAC1, ras-related C3 botulinum toxin substrate 1; KLF4, Kruppel-like factor-4; PLAC8, placenta-specific gene 8; PU.1, Spi-1 proto-oncogene; CD98, ectonucleoside triphosphate diphosphohydrolase 1; ID1, inhibitor of differentiationId-1; PKCɛ, protein kinase C ɛ; ERK2, extracellular regulated protein kinases 2; c-Myc, cellular myelocytomatosis viral oncogene; CXCL5, C-X-C motif chemokine 5; DUSP6, dual specificity phosphatase 6; MDM-2, murine double minute 2; p53, tumor protein 53