Effects of Astragalus polysaccharide on proliferation and Akt phosphorylation of the basal-like breast cancer cell line

2011 ◽  
Vol 9 (12) ◽  
pp. 1339-1346 ◽  
Author(s):  
MN Ye
Keyword(s):  
Breast Cancer ◽  
Cell Line ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Breast Cancer Cell Line ◽  
Cancer Cell Line ◽  
Akt Phosphorylation ◽  
Astragalus Polysaccharide ◽  
Basal Like Breast Cancer

scholarly journals Identification and transcript analysis of a novel wallaby (Macropus eugenii) basal-like breast cancer cell line

2008 ◽  
Vol 7 (1) ◽  
pp. 1 ◽  
Author(s):  
Julie A Sharp ◽  
Sonia L Mailer ◽  
Peter C Thomson ◽  
Christophe Lefèvre ◽  
Kevin R Nicholas
Keyword(s):  
Breast Cancer ◽  
Cell Line ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Breast Cancer Cell Line ◽  
Cancer Cell Line ◽  
Transcript Analysis ◽  
Macropus Eugenii ◽  
Basal Like Breast Cancer

scholarly journals BCRP and P-gp relay overexpression in triple negative basal-like breast cancer cell line: a prospective role in resistance to Olaparib

2015 ◽  
Vol 5 (1) ◽  
Author(s):  
Robin Dufour ◽  
Pierre Daumar ◽  
Emmanuelle Mounetou ◽  
Corinne Aubel ◽  
Fabrice Kwiatkowski ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Line ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Breast Cancer Cell Line ◽  
Triple Negative ◽  
Cancer Cell Line ◽  
Basal Like Breast Cancer

scholarly journals Cleavage of Syndecan-1 Promotes the Proliferation of the Basal-Like Breast Cancer Cell Line BT-549 Via Akt SUMOylation

2021 ◽  
Vol 9 ◽  
Author(s):  
Satomi Nadanaka ◽  
Yaqiang Bai ◽  
Hiroshi Kitagawa
Keyword(s):  
Breast Cancer ◽  
Cell Line ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Breast Cancer Cell Line ◽  
Cancer Cell Line ◽  
Sumo Modification ◽  
Physiological Importance ◽  
Mmp Inhibitor ◽  
Basal Like Breast Cancer

Basal-like breast cancer is characterized by an aggressive clinical outcome and presence of metastasis, for which effective therapies are unavailable. We have previously shown that chondroitin 4-O-sulfotransferase-1 (C4ST-1) controls the invasive properties of the basal-like breast cancer cell line BT-549 by inducing matrix metalloproteinase (MMP) expression through the N-cadherin/β-catenin pathway. Here we report that C4ST-1 controls the proliferation of BT-549 cells via the MMP-dependent cleavage of syndecan-1. Syndecan-1 is a membrane-bound proteoglycan associated with an aggressive phenotype and poor prognosis in breast cancer. In addition, the cleavage of syndecan-1 at a specific juxtamembrane cleavage site is implicated in the pathophysiological response in breast cancer. Knockout of C4ST-1 remarkably suppressed both the cleavage of syndecan-1 and proliferation of BT-549 cells. Kinases (AKT1, ERK1/2, PI3K, and STAT3) comprising cancer proliferative pathways are phosphorylated in C4ST-1 knockout cells at a level similar to that in parental BT-549 cells, whereas levels of phosphorylated S6 kinase and SUMOylated AKT (hyperactivated AKT observed in breast cancer) decreased in C4ST-1 knockout cells. An MMP inhibitor, GM6001, suppressed the small ubiquitin-like modifier (SUMO) modification of AKT, suggesting that cleavage of syndecan-1 by MMPs is involved in the SUMO modification of AKT. Forced expression of the cytoplasmic domain of syndecan-1, which is generated by MMP-dependent cleavage, increased the SUMO modification of AKT and global protein SUMOylation. Furthermore, syndecan-1 C-terminal domain-expressing BT-549 cells were more proliferative and sensitive to a potent SUMOylation inhibitor, tannic acid, compared with BT-549 cells transfected with an empty expression vector. These findings assign new functions to the C-terminal fragment of syndecan-1 generated by MMP-dependent proteolysis, thereby broadening our understanding of their physiological importance and implying that the therapeutic inhibition of syndecan-1 cleavage could affect the progression of basal-like breast cancer.

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