Galectin 3 acts as an enhancer of survival responses in H. pylori-infected gastric cancer cells.

Abstract:

:Galectin 3 (Gal-3) is upregulated in gastric epithelial cells as a host response to Helicobacter pylori infection. However, the significance of Gal-3 expression in H. pylori-infected cells is not well established. We analyzed Gal-3 intracellular expression, localization, and its effects in H. pylori-infected gastric epithelial cells. The predominantly nuclear confined Gal-3 was shown to be upregulated and exported out to the cytoplasm in H. pylori-infected AGS cells. The nuclear export was channeled through CRM-1 (exportin-1) protein. Interestingly, knock down of Gal-3 expression led to reduced NF-κB promoter activity and interleukin-8 (IL-8) secretion, suggesting its pro-inflammatory roles. Furthermore, Gal-3 was found to be pro-proliferative and anti-apoptotic in nature, as its knock down caused a reduction in cell proliferation and an increase in apoptosis, respectively. Taken together, our data suggest the expression and upregulation of Gal-3 as a critical endogenous event in H. pylori infection that interferes with various intracellular events, causing prolonged cell survival, which is characteristic in carcinogenesis.

journal_name

Cell Biol Toxicol

authors

Subhash VV,Ho B

doi

10.1007/s10565-016-9315-3

subject

Has Abstract

pub_date

2016-02-01 00:00:00

pages

23-35

issue

1

eissn

0742-2091

issn

1573-6822

pii

10.1007/s10565-016-9315-3

journal_volume

32

pub_type

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