Synthesis of sophocarpine triflorohydrazone and its proliferation inhibition and apoptosis induction activity in myeloma cells through Notch3‐p53 signaling activation

2020 ◽  
Author(s):  
Yong Wang ◽  
Wen Li ◽  
Fangmei Huang ◽  
Xiaojian Wu ◽  
Wenbin Chen ◽  
...  
Keyword(s):  
Proliferation Inhibition ◽  
Apoptosis Induction ◽  
Myeloma Cells ◽  
P53 Signaling ◽  
Signaling Activation

scholarly journals Apoptosis of mouse myeloma cells induced by curcumin via the Notch3‑p53 signaling axis

2018 ◽  
Author(s):  
Ying Zhang ◽  
Xin‑Yu Lin ◽  
Jiao‑Hui Zhang ◽  
Zheng‑Lu Xie ◽  
Hui Deng ◽  
...  
Keyword(s):  
Myeloma Cells ◽  
P53 Signaling ◽  
Signaling Axis ◽  
Mouse Myeloma

Hypophosphorylated Retinoic Acid Receptor Alpha Inhibits the Proliferation of Multiple Myeloma Cells

Blood ◽  
2012 ◽  
Vol 120 (21) ◽  
pp. 4990-4990
Author(s):  
Dong Zheng ◽  
Juan Li ◽  
Guo Xiaojuan ◽  
Zheng Chaoxu ◽  
Zhang Longjuan
Keyword(s):  
Multiple Myeloma ◽  
Retinoic Acid ◽  
Caspase 3 ◽  
Retinoic Acid Receptor ◽  
Control Group ◽  
G1 Arrest ◽  
Proliferation Inhibition ◽  
Retinoic Acid Receptor Alpha ◽  
Myeloma Cells ◽  
Acid Receptor

Abstract Abstract 4990 Background: Previous studies have shown that the effects of all-trans retinoic acid (ATRA) are mediated mainly through retinoic acid receptor alpha (RARα) and that the phosphorylation of a serine residue at amino acid 77 in the AF-1 domain of RARα was required for the basal activation function of RARα. In the present study, the effect of hypophosphorylated RARα(RARαS77A) in the proliferation of multiple myeloma(MM) was investigated. Methods: To determine whether RARαS77A would inhibit the proliferation of MM cells, RPMI8226 cells were transfected with constructing lentivirus-RARαS77A. The proliferation inhibition of ATRA and RARαS77A on MM cells were detectd by CCK-8. The molecular mechanisms of ATRA and RARαS77A on MM cells were explored by flow cytometer and western blotting. Results: The proliferation of RPMI8226 cells was inhibited by ATRA in a dose- and time-dependent manner. Compared with the control group, ATRA significantly arrested the cell cycle at the G1 phase (P<0. 05). The proliferation of MM cells transfected with lentivirus-RARαS77A was significantly inhibited compared with cells transfected with the control vector (p<0. 05). In addition, G1 arrest was significantly observed in MM cells transfected with lentivirus-RARαS77A (p<0. 05). The expression levels of retinoblastoma protein (Rb) and caspase-3 in the ATRA-treated and lentivirus-RARαS77A-transfected groups were increased compared with the control group. Conclusion: RARαS77A could mimic the proliferation inhibition and apoptosis promotion effects of ATRA on human RPMI8226 myeloma cells. Similar to ATRA, RARαS77A could induce G1 arrest by increasing the expression levels of Rb and caspase-3 in the anti-proliferation of MM cells. Disclosures: No relevant conflicts of interest to declare.

Mcl-1 Sequesters Pro-Apoptotic BH3-Only Bim To Inhibit Its Collaboration with Bax in Myeloma Cells.

Blood ◽  
2004 ◽  
Vol 104 (11) ◽  
pp. 789-789 ◽  
Author(s):  
Patricia Gomez-Bougie ◽  
Monique Clement ◽  
Philipe Juin ◽  
Regis Bataille ◽  
Martine Amiot
Keyword(s):  
Cell Survival ◽  
Plasma Cells ◽  
Myeloma Cell ◽  
Dynein Light Chain ◽  
Apoptosis Induction ◽  
Down Regulation ◽  
Myeloma Cells ◽  
Bh3 Domain ◽  
Major Interest ◽  
Apoptotic Effect

Abstract Multiple Myeloma is a fatal malignancy of B-cell origin characterized by the accumulation of plasma cells within the bone marrow. IL-6 is a major myeloma cell survival factor that induces the activation of both, Ras/MAP kinase and JAK/STAT pathways, the latter being involved in cell survival. Thus, IL-6 starvation or IL-6 signaling blockade by AG490 (a JAK 2 inhibitor) trigger apoptosis. In myeloma cells, others and us have shown that Mcl-1 is the major anti-apoptotic protein, since Mcl-1 antisenses induce apoptosis while Bcl-2 or Bcl-xL antisenses have no effect. In the present study, we examined the pro-apoptotic BH3-only molecule Bim which is implicated in apoptosis induced by growth factor deprivation. The three major Bim isoforms (EL, L and S) are expressed in viable human myeloma cell lines and are negatively regulated by IL-6. Blockade of IL-6 signaling induces the up-regulation of Bim isoforms concomitant to the down-regulation of Mcl-1. Of major interest, in viable myeloma cells, Bim is strongly associated to Mcl-1, to Bcl-2 and to a lesser extent to the dynein light chain, suggesting that Bim is always complexed in viable cells. Bim/Mcl-1 endogenous interaction is disrupted upon apoptosis induction, either by IL-6 starvation or AG 490 treatment. Of note, Bim/Bcl-2 complex is not affected under the same conditions. In parallel to disruption of Bim/Mcl-1 interaction and Bim release, Bax activation was observed. Microinjection of a peptide comprising the minimal BH3 domain from Bim triggered apoptosis in myeloma cells, confirming that free Bim might exert a direct pro-apoptotic effect in these cells. Therefore, in myeloma cells Mcl-1 neutralises Bim through endogenous complex formation. Under apoptosis induction, Mcl-1 drastic down-regulation leads to Bim release, which in turn exerts its pro-apoptotic function through Bax activation.

scholarly journals Quercetin nanoparticles display antitumor activity via proliferation inhibition and apoptosis induction in liver cancer cells

2017 ◽  
Vol 50 (4) ◽  
pp. 1299-1311 ◽  
Author(s):  
Ke-Wei Ren ◽  
Ya-Hua Li ◽  
Gang Wu ◽  
Jian-Zhuang Ren ◽  
Hui-Bin Lu ◽  
...  
Keyword(s):  
Liver Cancer ◽  
Antitumor Activity ◽  
Cancer Cells ◽  
Proliferation Inhibition ◽  
Apoptosis Induction ◽  
Liver Cancer Cells
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