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(−)‐Epigallocatechin‐3‐gallate induces cell apoptosis in chronic myeloid leukaemia by regulating Bcr/Abl‐mediated p38‐ MAPK / JNK and JAK 2/ STAT 3/ AKT signalling pathways
Author(s) -
Xiao Xiang,
Jiang Kaiming,
Xu Yunxiao,
Peng Hongling,
Wang Zhihua,
Liu Sufang,
Zhang Guangsen
Publication year - 2019
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/1440-1681.13037
Subject(s) - mapk/erk pathway , cancer research , imatinib , apoptosis , abl , cell growth , imatinib mesylate , k562 cells , protein kinase b , p38 mitogen activated protein kinases , myeloid leukemia , chemistry , stat , stat3 , kinase , signal transduction , microbiology and biotechnology , biology , tyrosine kinase , biochemistry
Summary Epigallocatechin‐3‐gallate ( EGCG ), a major polyphenolic constituent of green tea, possesses remarkable chemopreventive and therapeutic potential against various types of cancer, including leukaemia. However, the molecular mechanism involved in chronic myeloid leukaemia ( CML ), especially imatinib‐resistant CML cells, is not completely understood. In the present study, we investigated the effect of EGCG on the growth of Bcr/Abl+ CML cell lines, including imatinib‐resistant cell lines and primary CML cells. The results revealed that EGCG could inhibit cell growth and induce apoptosis in CML cells. The mechanisms involved inhibition of the Bcr/Abl oncoprotein and regulation of its downstream p38‐ MAPK / JNK and JAK 2/ STAT 3/ AKT pathways. In conclusion, we documented the anti‐ CML effects of EGCG in imatinib‐sensitive and imatinib‐resistant Bcr/Abl+ cells, especially T315I‐mutated cells.