ACA-28, an anticancer compound, induces Pap1 nuclear accumulation via ROS-dependent and -independent mechanisms in fission yeast

MicroPubl Biol. 2023 Aug 31;2023. doi: 10.17912/micropub.biology.000711. eCollection 2023.ABSTRACTThe nucleocytoplasmic transport of proteins is an important mechanism to control cell fate. Pap1 is a fission yeast nucleocytoplasmic shuttling transcription factor of which localization is redox regulated. The nuclear export factor Crm1/exportin negatively regulates Pap1 by exporting it from the nucleus to the cytoplasm. Here, we describe the effect of an anti-cancer compound ACA-28, an improved derivative of 1'-acetoxychavicol acetate (ACA), on the subcellular distribution of Pap1. ACA-28 induced nuclear accumulation of Pap1 more strongly than did ACA. ROS inhibitor N-acetyl-L-cysteine (NAC) partly antagonized the Pap1 nuclear accumulation induced by ACA-28. NAC almost abolished Pap1 nuclear localization upon H 2 O 2 , whereas leptomycin B (LMB)-mediated inhibition of Pap1 nuclear export was resistant to NAC. Collectively, ACA-28-mediated apoptosis in cancer cells may involve ROS-dependent and -independent mechanisms.PMID:37720683 | PMC:PMC10502506 | DOI:10.17912/micropub.biology.000711
Source: Cancer Control - Category: Cancer & Oncology Authors: Source Type: research