PURPOSE: Curcumin, a natural phytochemical, exhibits potent anticancer 
activities. Here, we sought to determine the molecular mechanisms underlying the 
cytotoxic effects of curcumin against human non-small cell lung cancer (NSCLC) 
cells.
METHODS: MTT assay and annexin-V/PI staining were used to analyze the effects of 
curcumin on the proliferation and apoptosis of A549 cells. The expression of 
microRNA-21 in curcumin-treated A549 cells was measured by quantitative 
real-time polymerase chain reaction assay. The protein level of phosphatase and 
tensin homolog (PTEN), a putative target of microRNA-21, was determined by 
Western blot analysis. Transfection of A549 cells with microRNA-21 mimic or PTEN 
small interfering RNA was performed to modulate the expression of microRNA-21 
and PTEN under the treatment of curcumin.
RESULTS: Curcumin at 20-40 μM inhibited cell proliferation and induced apoptosis 
in A549 cells. Curcumin treatment produced a dose-dependent and significant 
(P < 0.05) suppression of microRNA-21 expression, compared to untreated A549 
cells. Moreover, the protein level of PTEN, a putative target of microRNA-21, 
was significantly elevated in curcumin-treated A549 cells, as determined by 
Western blot analysis. Transfection of A549 cells with microRNA-21 mimic or PTEN 
small interfering RNA significantly (P < 0.05) reversed the growth suppression 
and apoptosis induction by curcumin, compared to corresponding controls.
CONCLUSIONS: Our data suggest a novel molecular mechanism in which inhibition of 
microRNA-21 and upregulation of PTEN mediate the anticancer activities of 
curcumin in NSCLC cells. Suppression of microRNA-21 may thus have therapeutic 
benefits against this malignancy.