References in periodicals archive ?
JP-1 Induces Apoptotic Sub-G1 Fraction in A549 Cells.
JP-1 Decreases CDK6 Protein and Activates the AMPK Pathway in A549 Cells.
JP-1 Induces p53 and Its Downstream Effectors p21 and BAX in A549 Cells.
JP-1 Increases the Transcription of miR-34a Accompanied by the Suppression of Its Downstream Targets Required for Proliferation and Apoptosis Resistance in A549 Cells.
JP-1 Downregulates the miR-34a Targets Controlling EMT and Inhibits Migration in A549 Cells.
Collectively, as shown in Scheme 1, the mechanism of action underlying the anticancer activities of JP-1 is proposed mainly through the activation of p53/miR-34a axis to modulate proteins related to cell-cycle regulation, apoptosis induction, and EMT.
JP-1 only had mild effect on the growth of HS68 human primary foreskin fibroblast cells as compared to its marked antiproliferation and apoptosis-induction activities in A549 cells.
It is deduced that the activation of AMPK by JP-1 might stabilize p53 through phosphorylation and acetylation, resulting in its accumulation.
In addition to the well-known p53 downstream targets such as p21 and BAX, we further unveil the effect of JP-1 on the transcription of miR-34a, which is recently regarded as a novel therapeutic target for LADC [23, 24].