Journal
FEBS LETTERS
Volume 590, Issue 3, Pages 358-368Publisher
WILEY
DOI: 10.1002/1873-3468.12057
Keywords
BCR-ABL; chronic myeloid leukemia; resistance; tyrosine kinase inhibitor
Funding
- Korean Health Technology R&D Project through the Korea Health Industry Development Institute (KHIDI)
- Ministry of Health and Welfare, Republic of Korea [HI11C1791, HI14C1466]
- Integrative Aging Research Center
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Some cases of chronic myelogenous leukemia are resistant to tyrosine kinase inhibitors (TKIs) independently of mutation in BCR-ABL, but the detailed mechanism underlying this resistance has not yet been elucidated. In this study, we generated a TKI-resistant CML cell line, K562R, that lacks a mutation in BCR-ABL. Interleukin-1 beta (IL-1 beta) was more highly expressed in K562R than in the parental cell line K562S, and higher levels of IL-1b contributed to the imatinib resistance of K562R. In addition, IL-1 beta secreted from K562R cells affected stromal cell production of CXCL11, which in turn promoted migration of K562R cells into the stroma. Thus, elevated IL-1 beta production from TKI-resistant K562R cells may contribute to TKI resistance by increasing cell viability and promoting cell migration.
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