Galectin-3 germline variant at position 191 enhances nuclear accumulation and activation of β-catenin in gastric cancer View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2011-12

AUTHORS

Seok-Jun Kim, Ji-Young Shin, Teak-Chin Cheong, Il-Ju Choi, Yeon Su Lee, Seok Hee Park, Kyung-Hee Chun

ABSTRACT

Mutation of galectin-3 at position 191 (rs4644) substituting proline to histidine (gal-3H(64)) resulted in the acquisition of resistance to drug-induced apoptosis by breast cancer cells. This study employed gastric cancer cells and patient tissues in attempts to elucidate how and why this mutation in galectin-3 (gal-3H(64)) enhances cancer progression, compared to wild type galectin-3 (gal-3P(64)). First, we prepared lenti-virus constructs containing gal-3P(64), gal-3H(64) and LacZ, and used them to infect galectin-3 null SNU-638 cells. We found that gal-3H(64) over-expression increases gastric cancer cell growth more than gal-3P(64) or LacZ over-expression. Also, gal-3H(64) over-expression conferred more resistance to cisplatin or 5-FU induced cytotoxicity than gal-3P(64). Gal-3H(64) also enhanced nuclear accumulation of β-catenin as well as increased expression of TCF-4 target genes, such as fascin-1 and c-Myc through the augmented promoter binding activity of TCF-4, than gal-3P(64). We also demonstrated stronger staining of β-catenin and galectin-3 in malignant tissues from gastric cancer patients with mutated galectin-3 at position 191 (gal-3 191) (A/A) (H(64)) and greater localization in the nucleus than in gal-3 191 A/C (P(64)) cancer patients. Taken together, we elucidated in this study that germline variant of gal-3H(64) increases nuclear accumulation of β-catenin and promotes TCF transcriptional activity and enhances more the galectin-3's role in gastric cancer progression. More... »

PAGES

743-750

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/s10585-011-9406-8

DOI

http://dx.doi.org/10.1007/s10585-011-9406-8

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1001878873

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/21750908


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