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Differential effect of NF‐κB activity on β‐catenin/Tcf pathway in various cancer cells
Author(s) -
Cho Hyun Hwa,
Song Ji Sun,
Yu Ji Min,
Yu Sung Sook,
Choi Sung Jong,
Kim Dong Heon,
Jung Jin Sup
Publication year - 2008
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2008.01.029
Subject(s) - nf κb , catenin , downregulation and upregulation , wnt signaling pathway , cancer research , signal transduction , beta catenin , colorectal cancer , chemistry , crosstalk , suppressor , cancer cell , biology , cancer , microbiology and biotechnology , biochemistry , genetics , gene , physics , optics
β‐Catenin/Tcf and NF‐κB pathways play an important role in biological functions. We determined the underlying mechanisms of differential interaction between two pathways in various human cancer cell lines. NF‐κB positively regulated β‐catenin/Tcf pathways in human glioblastoma, whereas it has an opposite effect on β‐catenin/Tcf pathways in colon, liver, and breast cancer cells. Expression of lucine zipper tumor suppressor 2 (lzts2) was positively regulated by NF‐κB activity in colon, liver, and breast cancer cells, whereas negatively regulated in glioma cells. Downregulation of lzts2 increased the β‐catenin/Tcf promoter activity and inhibited NF‐κB‐induced modulation of the nuclear translocation of β‐catenin. These data indicate that the differential crosstalk between β‐catenin/Tcf and NF‐κB pathway in various cancer cells is resulted from the differences in the regulation of NF‐κB‐induced lzts2 expression.