echemi logo
Product
  • Product
  • Supplier
  • Inquiry
    Home > Biochemistry News > Plant Extracts News > Inhibitory effect of silybin on growth related factors

    Inhibitory effect of silybin on growth related factors

    • Last Update: 2020-04-03
    • Source: Internet
    • Author: User
    Search more information of high quality chemicals, good prices and reliable suppliers, visit www.echemi.com
    2012-11-07 classification: the efficacy of 0 person review study shows that insulin-like growth factor (IGF) and related receptor data play an important role in stimulating cell proliferation and promoting malignant transformation of epithelial cells However, IGF activity is negatively regulated by igfbps-3, which has a high affinity for IGF Singh RP et al Fed with silybin (sb) (0.05% - 0.1%), found that the level of IGFBP-3 in the plasma of human prostate cancer DU145 xenograft mice increased by 4.6 times as compared with the control group, at the same time, the volume and weight of the tumor were significantly reduced, and no significant toxic and side effects were found in the experiment Furthermore, the concentration of silybin (sb) in mouse plasma (15.30gmol / ml) was used to act on DU145 cells The results also showed that IGFBP-3 in DU145 culture medium was significantly reduced and cell growth was inhibited Zix et al (171) used PC-3 cells of non androgen dependent prostate cancer It was found that sb could increase the level of IGFBP-3 protein by 6 times, its mRNA up-regulated by 9 times, and inhibit cell growth Animal experiments have proved that the level of silybin in blood (concentration of silybin 20gmol / ml) can be achieved Insulin receptor substrate-1 (IRS-1) is one of the key molecules in the downstream signal transduction events mediated by IGF-1 It has been found that sb can significantly inhibit IRS-1 activity with a inhibition rate of 70% Human epidermal growth factor (EGF) and its receptor family (erbB gene) play an important role in normal cell growth, but they play an important role in tumor Overexpression can lead to uncontrolled cell proliferation and tumorigenesis Erb EGF plays its role through egf-erbb1-shc-grb2-ras-raf-meki signal pathway, which is blocked by silybin Shanna y et al Treated prostate cancer LNCaP and DU145 cells with silibinin, the results showed that silibinin significantly inhibited the binding of EGF to ErbB1, EGF internalization and ErbB1 phosphorylation, but had no effect on the level of ErbB1 protein Zix et al Confirmed that SM can inhibit the constitutive activation of ErbB1 and tgf-a-induced activation in DU145 Further detection showed that the activity of she, a downstream signal transducer of ErbB1, was also down regulated, and cell cycle arrest and cell growth inhibition were observed Bhatia n et al [203 in the human epidermoid carcinoma A431 cell line with high expression of ErbB1, it was found that sb could effectively prevent the tyrosine phosphorylation of ErbB1 induced by EGF, but not change its protein level; it could inhibit the activation of she mediated by ErbB1, but also not change the protein level of she Silybin also inhibited EGF induced ERK1 / 2 activation.
    This article is an English version of an article which is originally in the Chinese language on echemi.com and is provided for information purposes only. This website makes no representation or warranty of any kind, either expressed or implied, as to the accuracy, completeness ownership or reliability of the article or any translations thereof. If you have any concerns or complaints relating to the article, please send an email, providing a detailed description of the concern or complaint, to service@echemi.com. A staff member will contact you within 5 working days. Once verified, infringing content will be removed immediately.

    Contact Us

    The source of this page with content of products and services is from Internet, which doesn't represent ECHEMI's opinion. If you have any queries, please write to service@echemi.com. It will be replied within 5 days.

    Moreover, if you find any instances of plagiarism from the page, please send email to service@echemi.com with relevant evidence.