Hyaluronidase activation of c-Jun N-terminal kinase is necessary for protection of L929 fibrosarcoma cells from staurosporine-mediated cell death

研究成果: Article同行評審

18 引文 斯高帕斯(Scopus)

摘要

Hyaluronidase counteracts the growth inhibitory function of transforming growth factor beta (TGF-β), whereas secretion of autocrine TGF-β and hyaluronidase is necessary for progression and metastasis of various cancers. Whether hyaluronidase and TGF-β1 induce resistance to staurosporine in L929 fibrosarcoma cells was investigated. When pretreated with TGF-β1 for 1-2 h, L929 cells resisted staurosporine apoptosis. In contrast, without pretreatment, hyaluronidase protected L929 cells fromstaurosporine apoptosis. Hyaluronidase rapidly activated p42/44 MAPK (or ERK) in L929 cells and TGF-β1 retarded the activation. Nonetheless, TGF-β1 synergistically increased hyaluronidase-mediated inhibition of staurosporine apoptosis. Hyaluronidase rapidly activated c-Jun N-terminal kinase (JNK1 and JNK2) in L929 cells in 20 min. Dominant negative JNK1, JNK2, and JNK3 abolished the hyaluronidase inhibition of staurosporine apoptosis, but not the TGF-β1 protective effect. Unlike the resistance to staurosporine, pretreatment of L929 cells with hyaluronidase is necessary to generate resistance to other anticancer drugs, including doxorubicin, daunorubicin, actinomycin D, and camptothecin, and the induced resistance was also blocked by dominant-negative JNKs. Together, hyaluronidase-mediated JNK activation is necessary to generate resistance to various anticancer drugs in L929 cells.

原文English
頁(從 - 到)278-286
頁數9
期刊Biochemical and Biophysical Research Communications
283
發行號2
DOIs
出版狀態Published - 2001

All Science Journal Classification (ASJC) codes

  • 生物物理學
  • 生物化學
  • 分子生物學
  • 細胞生物學

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