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Functions of Neutrophil Gelatinase-associated Lipocalin in the Esophageal
Carcinoma Cell Line SHEEC

Functions
of Neutrophil Gelatinase-associated Lipocalin in the Esophageal
Carcinoma Cell Line SHEEC


LI En-Min1,2*, XU Li-Yan2, CAI Wei-Jia2, XIONG Hua-Qi2, SHEN Zhong-Ying2, ZENG
Yi3

( 1Department of
Biochemistry and Molecular Biology, Shantou University Medical College, Shantou
515031, China;
2Institute of Oncologic Pathology, Shantou University Medical College, Shantou
515031, China;
3Institute of Virology, Chinese Academy of Preventive Medicine, Beijing 100052,
China )

Abstract
Neutrophil gelatinase-associated lipocalin (NGAL) is a novel member of the lipocalin family and may be a new human oncogene product, but function of

NGAL is not clear in the cancer. It was recently found that NGAL was overexpressed in the progression of malignant transformation from human immortalized esophageal

epithelial cell line SHEE to esophageal carcinoma cell line SHEEC. This indicated that cell line SHEEC was a good model for exploring functions of NGAL in the

carcinogenesis. The effects of blocking transcription of NGAL gene on invasion, division and proliferation of SHEEC cells were studied by antisense blocking RNA

technique and tumor formation in nude mice. The results showed that the antisense blocking of transcription of NGAL gene not only decreased effectively the activity of

MMP-9 and MMP-2 secreted by SHEEC cells, but suppressed significantly also the invasion of these cells in nude mice. However, the telomere length, the content of the

cellular topoisomeraseII-&agr; and cellular proliferation index (PI) of the SHEEC cells have not been changed markedly. These results indicate that NGAL is possibly

involved in invasion of tumor cells by regulating activity of MMP-9 and MMP-2, but is not apparently related with division and proliferation of tumor cells in SHEEC.

Key
words
sneutrophil gelatinase-associated lipocalin; esophageal carcinoma
cell; invasion of tumor cell; gelatinase; tumor formation in nude mice

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author:
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or 86-754-8532720; e-mail,[email protected],
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