BMC complementary medicine and therapies · 2022
Hinokiflavone induces apoptosis, cell cycle arrest and autophagy in chronic myeloid leukemia cells through MAPK/NF-κB signaling pathway.
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Qin Xiang, Chen Xi, Guo Ling, Liu Jing, Yang You, Zeng Yan, Li Cheng, Liu Wenjun, Ma Wenzhe
Аннотация
BACKGROUND: Chronic myeloid leukemia (CML) is a myeloproliferative tumor originating from hematopoietic stem cells, and resistance to tyrosine kinase inhibitors (TKI) has become a major cause of treatment failure. Alternative drug therapy is one of the important ways to overcome TKI resistance. Hinokiflavone (HF) is a C-O-C type biflavonoid with low toxicity and antitumor activity. This study investigated the antitumor effect and possible mechanisms of HF in CML cells.
METHODS: Cell viability was measured by CCK-8 assay. Cell apoptosis and cell cycle distribution were analyzed by flow cytometry. Western blotting was used to assess protein expression levels.
RESULTS: Our results showed that HF significantly inhibited the viability of K562 cells in a concentration- and time-dependent manner and induced G2/M phase arrest by up-regulating p21 and down-regulating Cdc2 protein. Furthermore, HF induced caspase-dependent apoptosis by activating JNK/p38 MAPK signaling pathway and inhibiting NF-κB activity. In addition, HF induced autophagy by increasing LC3-II expression and p62 degradation. Pretreatment with CQ, a late autophagy inhibitor, significantly increased the levels of LC3-II and p62 proteins and promoted cell survival.
CONCLUSION: HF shows a good anti-leukemia effect and is expected to become a potential therapeutic drug for CML.
METHODS: Cell viability was measured by CCK-8 assay. Cell apoptosis and cell cycle distribution were analyzed by flow cytometry. Western blotting was used to assess protein expression levels.
RESULTS: Our results showed that HF significantly inhibited the viability of K562 cells in a concentration- and time-dependent manner and induced G2/M phase arrest by up-regulating p21 and down-regulating Cdc2 protein. Furthermore, HF induced caspase-dependent apoptosis by activating JNK/p38 MAPK signaling pathway and inhibiting NF-κB activity. In addition, HF induced autophagy by increasing LC3-II expression and p62 degradation. Pretreatment with CQ, a late autophagy inhibitor, significantly increased the levels of LC3-II and p62 proteins and promoted cell survival.
CONCLUSION: HF shows a good anti-leukemia effect and is expected to become a potential therapeutic drug for CML.