BACKGROUND & OBJECTIVE: Bcl-2/E1B 19kDa interacting protein3-like (BNIP3L) gene 
is a tumor suppressor gene cloned from a human fetal liver cDNA library, which 
is located at 8p21, one of the high frequent regions of loss of heterozygosity 
(LOH) in lung carcinoma. BNIP3L protein can interact with antiapoptotic 
proteins, such as Bcl-2, Bcl-x(L), E1B19K, which promotes apoptosis. This study 
was designed to explore the correlation of alteration of expression and 
structure of BNIP3L gene with the progression of lung cancer.
METHODS: The expression and structure of BNIP3L gene in 4 lung cancer cell 
strains and 30 tissues were determined by SP immunohistochemistry, immunoblot, 
semi-quantitative reverse transcription-PCR (RT-PCR), PCR-single strain 
conformation polymorphism (PCR-SSCP).
RESULTS: (1) In 4 lung cancer cell strains, BNIP3L protein was not detected in 
A549, NCI-H460, NCI-H446, except for NCI-H520, in which the protein expression 
level was slightly lower than that in immortal bronchial epithelial cell strain 
HBE4-E6/E7. BNIP3L protein was observed in 46.7% (14/30) lung cancer tissues, 
while 100% (12/12) in normal lung tissues. The difference was significant in 
statistics (P< 0.05). (2) BNIP3L mRNA was detected in 4 lung cancer cell 
strains; and there existed no obvious discrepancy of the amount between these 
cell strains and HBE4-E6/E7. Absence or decrease of BNIP3L mRNA was observed in 
26.7%(8/30) of lung cancer tissues. The average quantity of BNIP3L mRNA was 
0.404+/-0.070 in lung cancer tissues, while 0.575+/-0.065 in paired normal lung 
tissues. The difference was significant in statistics (P< 0.05). In all the 
cancerous cell strains and tissues with BNIP3L mRNA, the products of RT-PCR were 
as long as those from their control samples in size, including the entire coding 
region, and no variation of BNIP3L gene structure such as absence, 
rearrangement, aberrant splicing were detected.(3) No point mutation was 
detected in all 6 exons of BNIP3L gene in 4 lung cancer cell strains and 30 
tissues.
CONCLUSION: BNIP3L protein expression was down-regulated in lung cancer, which 
might be involved in the occurrence and/or development of lung cancer. The 
down-regulation of BNIP3L protein expression in lung cancer was partly caused by 
the down-regulation of its transcription. The variation of gene structure may be 
not the reason of BNIP3L inactivity in lung cancer.