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GCA links TRAF6-ULK1-dependent autophagy activation in resistant chronic myeloid leukemia

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Title
GCA links TRAF6-ULK1-dependent autophagy activation in resistant chronic myeloid leukemia
Author(s)
Han, SH; Korm, S; Han, YG; Choi, SY; Kim, SH; Chung, HJ; Park, K; Kim, JY; Kyungjae Myung; Lee, JY; Hongtae Kim; Kim, DW
Publication Date
2019-12
Journal
AUTOPHAGY, v.15, no.12, pp.2076 - 2090
Publisher
TAYLOR & FRANCIS INC
Abstract
Imatinib is the first molecularly targeted compound for chronic myeloid leukemia (CML) capable to inhibit BCR-ABL kinase activity. However, recent clinical evidence indicates that a substantial proportion of CML patients exhibit BCR-ABL-dependent or independent resistance to imatinib. Despite the importance of imatinib resistance in CML, the underlying molecular mechanisms of this resistance are largely unknown. Here, we identified GCA (grancalcin) as a critical regulator of imatinib resistance in chronic phase CML via activation of autophagy. Mechanistically, we demonstrated that GCA activates TRAF6 ubiquitin ligase activity to induce Lys63 ubiquitination of ULK1, a crucial regulator of autophagy, resulting in its stabilization and activation. We also highlighted the role of GCA-TRAF6-ULK1 autophagy regulatory axis in imatinib resistance. Our findings represent the basis for novel therapeutic strategies against CML. © 2019 Informa UK Limited, trading as Taylor & Francis Group
URI
https://pr.ibs.re.kr/handle/8788114/6727
ISSN
1554-8627
Appears in Collections:
Center for Genomic Integrity(유전체 항상성 연구단) > Journal Papers (저널논문)
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