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Effects of calreticulin on FUT1 expression and beta1 integrin fucosylation in different cancer cells
Author(s) -
Weng YiCheng,
Chien YinChieh,
Lu KuanYing,
Lee Hsinyu
Publication year - 2016
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.30.1_supplement.1227.5
Subject(s) - gene knockdown , fucosylation , calreticulin , cancer research , cancer cell , chemistry , integrin , microbiology and biotechnology , cell migration , cell growth , cell , cancer , biology , apoptosis , biochemistry , endoplasmic reticulum , genetics , glycoprotein , glycan
Calreticulin (CRT) is a multifunctional ER chaperon protein. We had demonstrated that knockdown of CRT may suppress cell proliferation and migration in J82 bladder cancer cells. We further revealed that CRT stabilized the mRNA of fucosyltransferase1 (FUT1), which leads to an enhancement of fucosylation and the subsequent activation of beta1 integrin. Previous studies had demonstrated that knockdown of CRT suppress cell proliferation and migration in both PC3 prostate cancer cells and AGS gastric cancer cells. However, the effects of CRT on FUT1 expression and beta1 integrin fucosylation have not been investigated in these cells. In this study, we demonstrated that knockdown of CRT decreased the expression levels of FUT1 in PC3 cells and AGS cells. Furthermore, the fucosylation levels of beta1 integrin were significantly down regulated in these CRT knockdown cells. However, mRNA stability of FUT1 was not affected in either cell lines. These results suggested that CRT might affect the fucosylation of beta1 integrin in both PC3 cells and AGS cells. However, a different molecular mechanism was involved while compared to J82 bladder cancer cells. Taken together, our observations imply that CRT may regulate FUT1 expression differently between different cancer cells.