Previous reports suggested that protoapigenone showed remarkable antitumor 
activities against a broad spectrum of human cancer cell lines, but had no 
effect on human lung adenocarcinoma A549 cell. The lack of effective remedies 
had necessitated the application of new therapeutic scheme. A novel compound 
RY10-4 which has the similar structure close to protoapigenone showed better 
antitumor activity. Treatment with RY10-4 inhibited the expression of 
pro-caspase-3, pro-caspase-9, Bcl-2 as well as phosphorylation of signal 
transducer and activator of transcription-3 (p-STAT3). It also reduced the 
expressions of matrix metalloproteinase-2 (MMP-2), matrix metalloproteinase-9 
(MMP-9) and increases the expressions of reversion-inducing cysteine-rich 
protein with kazal motifs (RECK), as well as tissue inhibitor of 
metalloproteinase (TIMP) via inhibiting STAT3 by activating the 
mitogen-activated protein (MAP) kinases (the c-Jun N-terminal kinase (JNK), the 
p38 and extracellular signal-regulated kinase (ERK)) in A549 cells treated with 
RY10-4. Moreover, the cytotoxic effect of RY10-4 was induction of apoptosis in 
A549 cells by enhancing production of reactive oxygen species (ROS). Taken 
together, the observations suggested that RY10-4 had affected Bcl-2 family 
members, caspases, MMPs, TIMPs expressions and ROS production via inhibiting 
STAT3 activities through ERK and p38 pathways in A549 cells.