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A novel apoptotic pathway as defined by lectin cellular initiation.

Abstract：

:In this study of lectin-induced apoptosis we found that wheat germ agglutinin (WGA) initiated an accelerated type of programmed cell death developing after only 30 min of incubation with tumor cells. To analyze possible mechanisms, studies were focused using the WGA lectin whose carbohydrate specificity is well defined. We found that WGA could induce apoptosis by binding to either N-acetylneuraminic acid or N-acetylglucosamine (GlcNAc) on the cell surface of normal and malignant cells. We also showed that it is unlikely that WGA triggers apoptosis by binding to the carbohydrate portion of Fas. CrmA gene transfection did not inhibit WGA-mediated apoptosis of Jurkat cells. In addition, Jurkat-R cells selected for resistance to Fas signaled apoptosis manifested high sensitivity to WGA as did Fas-negative BL6 melanoma cells. WGA-induced apoptosis is also caspase-3-independent and was found to be triggered via a mitochondrial pathway. WGA induced a loss of transmembrane potential, disruption of the inner mitochondria membrane, and release of cytochrome c and caspase-9 activation after 30 min of cell interaction. Interestingly, Bcl-2 gene transfection did not affect sensitivity of Jurkat cells to WGA. The Jurkat-R subline that has been shown to be Bax and Bak deficient and resistant to various apoptotic signals was highly sensitive to WGA-induced apoptosis. In summary, WGA triggers a unique pattern of apoptosis that is extremely fast, Fas- and caspase-3-independent, and is mediated via a mitochondrial pathway. However, its mitochondrial component is unrestrained by the loss of Bax and Bak or the upregulation of Bcl-2 expression.

journal_name

Biochem Biophys Res Commun

journal_title

Biochemical and biophysical research communications

authors

Gastman B,Wang K,Han J,Zhu ZY,Huang X,Wang GQ,Rabinowich H,Gorelik E

doi

10.1016/j.bbrc.2004.02.043

subject

Has Abstract

pub_date

2004-03-26 00:00:00

pages

263-71

issue

1

eissn

0006-291X

issn

1090-2104

pii

S0006291X04002888

journal_volume

316

pub_type

杂志文章

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