J Lung Cancer.  2007 Dec;6(2):74-77. 10.6058/jlc.2007.6.2.74.

Mutational Analysis of Pro-apoptotic BNIP3 Gene in Non- Small Cell Lung Cancers

• Lee SH
• Lee SH

• KMID: 1820248
• DOI: http://doi.org/10.6058/jlc.2007.6.2.74

Abstract

PURPOSE : Cell death deregulation is a hallmark of human cancers. BNIP3, which was initially identified as a pro-apoptotic member of the Bcl-2 family, plays an important role in apoptosis, necrosis and autophagy. This study was conducted to explore whether mutation of the BNIP3 gene is a characteristic of human non-small cell lung cancers (NSCLC).
MATERIALS AND METHODS
: In the current study, we used polymerase chain reaction (PCR), single-strand conformation polymorphism (SSCP), and DNA sequencing to detect somatic mutations in the DNA sequences encoding the BH3 (Bcl-2 homology3) and TM (transmembrane) domains that are important to the cell death function of BNIP3 in 48 NSCLCs.
RESULTS
: SSCP analysis revealed no evidence of somatic mutation in the DNA sequences encoding the BH3 and TM domains of the human BNIP3 gene in the 48 NSCLCs evaluated in this study.
CONCLUSION
: The data presented here indicate that the pro-apoptotic BNIP3 gene may not be somatically mutated in human NSCLCs, which suggests that mutational events of the BNIP3 gene may not be involved in the mechanisms by which NSCLCs evade cell death

Keyword

Non-small cell lung cancer; BNIP3; Cell death; Mutation

MeSH Terms

Apoptosis
Autophagy
Base Sequence
Carcinoma, Non-Small-Cell Lung
Cell Death
Humans
Lung Neoplasms*
Lung*
Necrosis
Polymerase Chain Reaction
Polymorphism, Single-Stranded Conformational
Sequence Analysis, DNA

Figure

• 

  Fig. 1. Representative SSCP of BNIP3 gene in the non-small cell lung cancers. The exon 4 of the BNIP3 gene was amplified by PCR using a specific primer set. The PCR products from the representative cases of non-small cell lung cancers were visualized on SSCP. SSCP of DNA from the non-small cell lung cancers (T) shows no aberrant bands as compared to SSCPs from the normal tissues (N).

Reference

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