IGF-I plus E2 induces proliferation via activation of ROS-dependent ERKs and JNKs in human breast carcinoma cells.
作者： Cheng-Wei Lin , Liang-Yo Yang , Shing-Chuan Shen , Yen-Chou Chen
DOI: 10.1002/JCP.21061
关键词:
摘要: Induction of 17beta-estradiol (E2) and insulin-like growth factor-I (IGF-I) has been detected in breast carcinoma, however the interaction between E2 IGF-I proliferation carcinoma cells is still unclear. In present study, we found that enhances E2-induced MCF-7 human accordance with stimulation colony formation via a soft agar assay. Activation insulin receptor substrate-1 (IRS-1) protein extracellular signal-related kinases (ERKs) c-Jun N-terminal (JNKs), but not p38 mitogen-activated kinase (MAPK), phosphorylation induction was treated plus (E2/IGF-I). E2/IGF-I-induced blocked by chemical inhibitors ERKs (PD98059) JNKs (SP600125). An increase expression E2/IGF-I-treated cells, this inhibited PD98059 SP600125. Transfection dominant negative MEKK JNK plasmids significantly reduced suppression expression. peroxide production N-acetyl-L-cysteine (NAC) Tiron (TIR) addition cell blocking JNKs, protein. Additionally, 3-OH flavone, baicalein, quercetin showed effective inhibitory activities against through suppressing proliferative events such as IRS-1, ERKs, proteins, formation. These results indicate interacts to promote ROS-dependent MAPK activation The structure-related inhibition flavonoids elucidated.
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