Objective:To study the effects and possible mechanism of action of KL1 protein in human non-small cell lung cancer cells A549. Methods:Western blot was used to detect the overexpression of KL or KL1 in A549 cells transfected with pcDNA3.1-MYC-KL1 or pcDNA3.1-MYC-KL. MTT assay,colony-forming assay and flow-cytometry analysis were designed to determine the change of cell growth,proliferation and apoptosis of A549 cells mediated by KL or KL1, respectively. Effects on the phosphorylation of ERK1/2 in the middle and lower target site of the basic fibroblast growth factor(bFGF) signaling pathway were detected by Western blot after transfection. Results:After transfected 48 h,exogenous KL or KL1 was overexpressed significantly in A549 cells (both P < 0.01). Compared with the control group,the cell growth was inhibited in A549 cells after transfected with KL1 (P < 0.01),the proliferation was remarkably inhibited (P < 0.01)and the apoptosis was promoted significantly(P < 0.01). KL1 overexpression in A549 cells was associated with reduced bFGF-induced phosphorylation of ERK1/2 (P < 0.01). There was no signifcant difference between overexpressed KL and KL1 in cell growth,proliferation and activation of bFGF signal pathway (P > 0.05). Conclusion:The KL and KL1 have a similar signifcant ability to inhibit the growth,proliferation and promote the apoptosis of A549 cells. This may be due to the same ability to inhibit bFGF pathway. Thus,KL1 may be the main functional fragment of the KL protein.