Aim: To observe the effects of a novel all-trans retinoid acid (ATRA) derivative, N-(3-trifluoromethyl-phenyl)-retinamide (ATPR), on lung adenocarcinoma A549 cells and to explore the potential mechanism of ATPR inhibitingof A549 cell migration. Materials and
Methods: The cytotoxicity of ATRA and ATPR on A549 cells was assessedusing MTT assay. Wound healing assays were used to analyze the influences of ATRA, ATPR, ML-7 (a highlyselective inhibitor of myosin light chain kinase (MLCK)), PMA (an activator of MAPKs) and PD98059 (a selectiveinhibitor of ERK1/2) on the migration of A549 cells. Expression of MLCK and phosphorylation of myosin lightchain (MLC) were assessed by Western blotting.
Results: ATRA and ATPR inhibited the proliferation of A549cells in a dose- and time-dependent manner, and the effect of ATPR was much more remarkable comparedwith ATRA. Relative migration rate and migration distance of A549 cells both decreased significantly aftertreatment with ATPR or ML-7. The effect on cell migration of PD98059 combining ATPR treatment was morenotable than that of ATPR alone. Moreover, compared with control groups, the expression levels of MLCK andphosphorylated MLC in A549 cells were both clearly reduced in ATRA and ATPR groups.
Conclusions: ATPRcould suppress the migration and invasion of A549 cells, and the mechanism might be concerned with downregulatingthe expression of MLCK in the ERK-MAPK signaling pathway, pointing to therapeutic prospects inlung cancer.