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Platycodin D inhibits proliferation, migration and induces chemosensitization through inactivation of the NF ‐κB and JAK 2/ STAT 3 pathways in multiple myeloma cells
Author(s) -
Wu Di,
Zhang Wei,
Chen Ying,
Ma Hong,
Wang Mengchang
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 - 10.1111/1440-1681.13145
Subject(s) - chemistry , cell growth , flow cytometry , bortezomib , stat protein , stat , western blot , apoptosis , cancer research , microbiology and biotechnology , stat3 , biology , immunology , multiple myeloma , biochemistry , gene
Multiple myeloma ( MM ) is a malignancy characterized by the proliferation of malignant plasma cells. Platycodin D ( PLD ) is a triterpenoid saponin that exerts anti‐tumour activity through multiple mechanisms. However, the role of PLD in MM remains unknown. Here, we investigated the effect of PLD on MM cell lines NCI ‐H929 and U266B1, and elucidated the underlying molecular mechanism. Cell Counting Kit‐8 assay showed that the proliferation of NCI ‐H929 and U266B1 cells was significantly decreased after PLD treatment. Transwell assay confirmed that PLD treatment suppressed migration of NCI ‐H929 and U266B1 cells. Flow cytometry results indicated that the apoptotic rates of bortezomib ( BTZ )‐treated NCI ‐H929 and U266B1 cells were markedly increased after PLD treatment. Western blot analysis revealed that bcl‐2 expression was decreased, while bax expression was increased in PLD ‐treated NCI ‐H929 and U266B1 cells compared with that in BTZ ‐treated cells. Furthermore, PLD treatment blocked the activation of nuclear factor‐kappa B ( NF ‐κB) and Janus kinase 2 ( JAK 2)/signal transducer and activator of transcription 3 ( STAT 3) signalling pathways in NCI ‐H929 cells. Taken together, these data showed that PLD inhibited proliferation and migration, and enhanced chemosensitization to BTZ through inactivation of the NF ‐κB and JAK 2/ STAT 3 pathways in MM cell lines. These findings indicated that PLD might serve as a novel therapeutic agent for the treatment of MM .