Objectives:The antitumor effects of pyropheophorbide-αmethyl ester-mediated photodynamic therapy(MPPa-PDT)were observed in several cancers.The objective of this investigation was to examine the antineoplastic efficacy...Objectives:The antitumor effects of pyropheophorbide-αmethyl ester-mediated photodynamic therapy(MPPa-PDT)were observed in several cancers.The objective of this investigation was to examine the antineoplastic efficacy of MPPa-PDT acting on lung carcinoma A549 cells and further elaborate mechanisms.Methods:The viability of A549 cells was examined with cell counting kit-8 after MPPa-PDT disposal.Hoechst 33342 staining,monodansylcadaverine(MDC)staining,and transmission electron microscopy were employed to observe apoptotic bodies and autophagic vesicles.Flow cytometry with Annexin V/propidium iodide(PI)labeling objectively assessed cell death.The expression of associated proteins,including Caspase-3,Beclin-1,LC-3II,and mitogen-activated protein kinase(MAPK)families concluding c-jun NH2-terminal kinase(JNK),p38 MAPK,and extracellular signal-regulated kinase 1/2(ERK)were identified by Western blotting.Results:Prolonged exposure to MPPa-PDT gradually decreased lung cancer A549 cell viability.Apoptosis and autophagy activity were higher in the MPPa-PDT cohort in comparison to the control group.Meanwhile,autophagy inhibition enhanced cell-killing efficacy apparently.Besides,the JNK and p38 MAPK pathways were implicated in MPPa-PDT-triggered apoptosis and autophagy.Conclusions:This study demonstrated that JNK and p38 MAPK were engaged in MPPa-PDT-mediated apoptosis and autophagy in lung carcinoma A549 cells.展开更多
基金supported by XiaoganCity Natural Science Foundation of China (Grant/AwardNo. XGKJ2022010004).
文摘Objectives:The antitumor effects of pyropheophorbide-αmethyl ester-mediated photodynamic therapy(MPPa-PDT)were observed in several cancers.The objective of this investigation was to examine the antineoplastic efficacy of MPPa-PDT acting on lung carcinoma A549 cells and further elaborate mechanisms.Methods:The viability of A549 cells was examined with cell counting kit-8 after MPPa-PDT disposal.Hoechst 33342 staining,monodansylcadaverine(MDC)staining,and transmission electron microscopy were employed to observe apoptotic bodies and autophagic vesicles.Flow cytometry with Annexin V/propidium iodide(PI)labeling objectively assessed cell death.The expression of associated proteins,including Caspase-3,Beclin-1,LC-3II,and mitogen-activated protein kinase(MAPK)families concluding c-jun NH2-terminal kinase(JNK),p38 MAPK,and extracellular signal-regulated kinase 1/2(ERK)were identified by Western blotting.Results:Prolonged exposure to MPPa-PDT gradually decreased lung cancer A549 cell viability.Apoptosis and autophagy activity were higher in the MPPa-PDT cohort in comparison to the control group.Meanwhile,autophagy inhibition enhanced cell-killing efficacy apparently.Besides,the JNK and p38 MAPK pathways were implicated in MPPa-PDT-triggered apoptosis and autophagy.Conclusions:This study demonstrated that JNK and p38 MAPK were engaged in MPPa-PDT-mediated apoptosis and autophagy in lung carcinoma A549 cells.